This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Jackson, W. F. Search for Related Content PubMed PubMed Citation Articles by Jackson, W. F. Related Collections Calcium cycling/excitation-contraction coupling Cell signalling/signal transduction Hypertension - basic studies Ion channels/membrane transport

(Hypertension. 2000;35:173.)
© 2000 American Heart Association, Inc.

Workshop

Ion Channels and Vascular Tone

William F. Jackson

From the Department of Biological Sciences, Western Michigan University, Kalamazoo, Mich.

Correspondence to Dr William F. Jackson, Department of Biological Sciences, Western Michigan University, 3169 Wood Hall, Kalamazoo, MI 49008. E-mail jackson{at}wmich.edu

	Abstract

Top Abstract Introduction Regulation of Vascular Tone... KATP Channels and Vascular... BKCa Channels and Vascular... KV Channels and Vascular... KIR Channels and Vascular... Cl- Channels and Vascular... Store-Operated and Stretch... Summary References

 
Abstract—Ion channels in the plasma membrane of vascular muscle cells that form the walls of resistance arteries and arterioles play a central role in the regulation of vascular tone. Current evidence indicates that vascular smooth muscle cells express at least 4 different types of K⁺ channels, 1 to 2 types of voltage-gated Ca²⁺ channels, 2 types of Cl^- channels, store-operated Ca⁺ (SOC) channels, and stretch-activated cation (SAC) channels in their plasma membranes, all of which may be involved in the regulation of vascular tone. Calcium influx through voltage-gated Ca²⁺, SOC, and SAC channels provides a major source of activator Ca²⁺ used by resistance arteries and arterioles. In addition, K⁺ and Cl^- channels and the Ca²⁺ channels mentioned previously all are involved in the determination of the membrane potential of these cells. Membrane potential is a key variable that not only regulates Ca⁺² influx through voltage-gated Ca²⁺ channels, but also influences release of Ca²⁺ from internal stores and Ca²⁺- sensitivity of the contractile apparatus. By controlling Ca²⁺ delivery and membrane potential, ion channels are involved in all aspects of the generation and regulation of vascular tone.

Key Words: muscle, smooth, vascular • arterioles • potassium channels • calcium channels • vascular resistance • vasoconstriction

	Introduction

Top Abstract Introduction Regulation of Vascular Tone... KATP Channels and Vascular... BKCa Channels and Vascular... KV Channels and Vascular... KIR Channels and Vascular... Cl- Channels and Vascular... Store-Operated and Stretch... Summary References

 
Vascular tone, the contractile activity of vascular smooth muscle cells in the walls of small arteries and arterioles, is the major determinant of the resistance to blood flow through the circulation. Thus, vascular tone plays an important role in the regulation of blood pressure and the distribution of blood flow between and within the tissues and organs of the body. Regulation of the contractile activity of vascular smooth muscle cells in the systemic circulation is dependent on a complex interplay of vasodilator and vasoconstrictor stimuli from circulating hormones, neurotransmitters, endothelium-derived factors, and blood pressure. All of these signals are integrated by vascular muscle cells to determine the activity of the contractile apparatus of the muscle cells and hence the diameter and hydraulic resistance of a blood vessel. Ion channels play a central role in this process. Like all muscle cells, vascular smooth muscle uses Ca²⁺ as the trigger for contraction. Calcium influx through channels in the plasma membrane and Ca²⁺ release from intracellular stores are the major source of activator Ca²⁺. In addition, the movement of ions through ion channels determines, to a large extent, membrane potential. Membrane potential, along with cytosolic Ca²⁺ concentration, regulates and modulates the influx^{1 2} and release^{3 4 5} of Ca²⁺ through ion channels and the sensitivity of the contractile machinery to Ca²⁺.⁶ Vascular smooth muscle cells express 4 different types of K⁺ channels,^{7 8} 1 to 2 types of voltage-gated Ca²⁺ channels,^{1 2} 2 types of Cl^- channels,^{9 10 11} store-operated Ca⁺ channels,^{12 13} and stretch-activated cation channels^{14 15 16} in their plasma membranes, all of which may be involved in the regulation of vascular tone. These channels will serve as the focus of this review, with particular emphasis on regulation of vascular tone in the microcirculation. The reader is referred to several recent reviews for information about intracellular ion channels^{13 17 18} and ion channels in endothelial cells,¹⁹ which also are involved in the determination of vascular tone.

	Regulation of Vascular Tone by K+ Channels and Voltage-Gated Ca+ Channels

Top Abstract Introduction Regulation of Vascular Tone... KATP Channels and Vascular... BKCa Channels and Vascular... KV Channels and Vascular... KIR Channels and Vascular... Cl- Channels and Vascular... Store-Operated and Stretch... Summary References

 
Potassium channels are the dominant ion conductive pathways in vascular muscle cells.^{7 8} As such, their activity importantly contributes to determination and regulation of membrane potential and vascular tone.^{7 8} The electrochemical gradient for K⁺ ions is such that opening of K⁺ channels results in diffusion of this cation out of the cells and membrane hyperpolarization (Figure 1). Closure of K⁺ channels has the opposite effect (Figure 1).

View larger version (28K): [in this window] [in a new window]   Figure 1. K+ channels and vascular tone. Schematic of a vascular smooth muscle cell (top) and cross sections through an arteriole (bottom) that shows that opening K+ channels leads to diffusion of K+ ions out of the cell, membrane hyperpolarization, closure of voltage-gated Ca2+ channels, decreased intracellular Ca2+, etc (see text), which leads to vasodilatation. Closure of K+ channels has the opposite effect. Modified from Jackson.8

Voltage-gated Ca²⁺ channels play a central role in the regulation of vascular tone by membrane potential^{1 2} : hyperpolarization closes these channels and leads to vasodilatation, whereas depolarization opens them, which results in vasoconstriction (Figure 1). Dihydropyridine-sensitive L-type voltage-gated Ca²⁺ channels appear to be dominant in most vascular muscle cells,^{1 2} although T-type Ca²⁺ channels have been reported.² In the microcirculation, L-type Ca²⁺ channels appear to play a particularly important role in myogenic reactivity^{20 21 22} and vasomotion.^{20 23 24} Voltage-gated Ca²⁺ channels are modulated by several signaling systems.² They appear to be activated by vasoconstrictors that activate the protein kinase C pathway.² Vasodilators that stimulate production of cAMP and activate protein kinase A have been reported to both activate and inhibit these channels.² Voltage-gated Ca²⁺ channels are inhibited by increases in intracellular Ca²⁺ and activation of cGMP-dependent protein kinase.² Thus, these ion channels are poised to contribute to an important degree to the neural, humoral, and local regulation of vascular tone.

Membrane potential not only regulates voltage-gated Ca²⁺ channels, but also appears to influence inositol 1,4,5-trisphosphate–induced release of Ca²⁺ from intracellular stores^{3 4 5} and the Ca²⁺ sensitivity of the contractile apparatus.⁶ Thus, by their dominance in setting membrane potential, K⁺ channels play a central role in determination and regulation of vascular tone. In the microcirculation, as in other vascular muscles, we have identified functional expression of 4 different classes of K⁺ channels (see Figure 1): ATP-sensitive K⁺ (K_ATP) channels, large-conductance Ca²⁺- activated K⁺ (BK_Ca) channels, voltage-activated K⁺ (K_V) channels, and inward rectifier K⁺ (K_IR) channels.^{8 25 26 27}

	KATP Channels and Vascular Tone

Top Abstract Introduction Regulation of Vascular Tone... KATP Channels and Vascular... BKCa Channels and Vascular... KV Channels and Vascular... KIR Channels and Vascular... Cl- Channels and Vascular... Store-Operated and Stretch... Summary References

 
ATP-sensitive K⁺ channels were first described by Noma²⁸ in cardiac myocytes. Subsequent studies by other investigators have identified currents through similar channels in many other cell types, including vascular smooth muscle cells (see references ²⁹ through –³² for recent reviews). These channels close as intracellular ATP concentration increases; hence, their name. However, as mentioned below, K_ATP channels are also regulated by several signal transduction pathways independent from changes in ATP. Thus, other regulatory pathways may be more physiologically important.

Early studies showed that glibenclamide, a selective K_ATP channel blocker, caused arteriolar constriction in several microcirculatory beds in a number of species, including humans.^{33 34 35 36 37 38 39} These data support the hypothesis that K_ATP channels may be active in the microcirculation under resting conditions. Glibenclamide has been reported to have no effect on resting vascular resistance in several vascular beds.^{40 41 42 43} The reason for these differences is not obvious and has not been experimentally explored. The differences may indicate species or regional differences in the activity and regulation of these channels or methodological differences among the studies described above.

Several studies have shown that K_ATP channel agonists such as cromakalim and pinacidil dilate arterioles,^{7 31 33 34 44} which provides evidence that recruitable K_ATP channels also are present in arteriolar muscle cells. In addition, arteriolar dilation induced by adenosine, prostacyclin, and isoproterenol is mediated, in part, by opening of K_ATP channels.^{33 34} These functional studies provided evidence that this class of ion channel plays a crucial role in the regulation of vascular tone in the microcirculation.

The open K_ATP channels implied by the functional experiments noted above have recently been confirmed by electrophysiological measurements in single, isolated arteriolar muscle cells with the perforated patch technique.²⁷ Superfusion of either hamster or rat cremasteric arteriolar muscle cells with glibenclamide (1 µmol/L), inhibited currents between -60 and -30 mV (normal range of resting membrane potential), decreased whole-cell membrane conductance, and depolarized current-clamped cells by >10 mV.²⁷ These experiments provided the first direct evidence that open K_ATP channels exist in resting arteriolar muscle cells. Thus, K_ATP channels play an important role in the regulation of resting membrane potential and, hence, tone of arteriolar muscle cells. They also appear to participate in the mechanism of action of vasodilators such as adenosine and prostacyclin through cAMP/protein kinase A–dependent⁷ and –independent³⁴ mechanisms. Furthermore, some vasoconstrictors may act, in part, by closure of K_ATP channels through a mechanism that involves protein kinase C.^{7 36} K_ATP channels have been implicated in functional hyperemia,^{35 39 40} reactive hyperemia,^{37 41 42} and responses to reductions in blood flow⁴³ in several skeletal muscle models. Responses of arterioles and resistance arteries to K_ATP channel agonists are blunted during experimental diabetes mellitus,^{45 46 47 48} which suggests a role for these channels in the causation of or as a consequence of vascular complications present in this disease.

	BKCa Channels and Vascular Tone

Top Abstract Introduction Regulation of Vascular Tone... KATP Channels and Vascular... BKCa Channels and Vascular... KV Channels and Vascular... KIR Channels and Vascular... Cl- Channels and Vascular... Store-Operated and Stretch... Summary References

 
Large-conductance BK_Ca channels are found in most cells.⁴⁹ These channels are activated by increases in intracellular Ca²⁺ and membrane depolarization.^{7 50} In small arteries that display myogenic tone, activity of BK_Ca channels has been reported to contribute to resting membrane potential: blockade of the channels with iberiotoxin or tetraethyl ammonium (TEA) ions leads to membrane depolarization and vasoconstriction.^{1 7 51 52} Nelson and colleagues have championed the idea that BK_Ca channels play a central role in the regulation of vascular tone due to focal increases in subsarcolemmal Ca²⁺ (ie, Ca²⁺ sparks) by Ca²⁺ released through ryanodine receptors in the sarcoplasmic reticulum.^{17 51 53}

In the microcirculation, despite substantial resting myogenic tone, BK_Ca channels appear to be silent^{25 27 54 55} ; application of iberiotoxin or TEA has no effect on resting arteriolar diameter in vivo,^{25 54 55} and neither agent affects membrane potential or whole-cell K⁺ currents in single cells in vitro.^{8 27} This lack of apparent BK_Ca channel activity appears to arise because the channels present in the membranes of these cells have a high calcium threshold. That is, high levels of Ca²⁺, on the order of 3 to 10 µmol/L, are required for channel activity in the physiological range of membrane potentials (-60 to -30 mV) in relaxed cells.²⁵ Despite this high threshold, these channels are activated in the microcirculation during active vasoconstriction by agents such as norepinephrine and elevated oxygen tension.²⁵ Thus, BK_Ca channels appear to play a negative feedback role to limit active vasoconstriction and prevent vasospasm. In addition, these channels may be activated by vasodilators that act through the cGMP and cAMP cascades,^{7 54} epoxides of arachidonic acid⁵⁶ and CO.^{57 58 59} These channels may be closed by 20-OH arachidonic acid produced by cytochrome P450_4a.⁶⁰ Furthermore, vasodilators and vasoconstrictors may influence the frequency and amplitude of Ca²⁺ sparks and thus influence BK_Ca channel activity.^{53 61 62} Finally, expression of BK_Ca channels in vascular smooth muscle membranes is increased during hypertension^{63 64 65 66 67} and has been proposed to occur as a negative feedback response to the increased vascular reactivity observed in hypertension.⁶⁷ Thus, BK_Ca channels play an important role in regulation of vascular tone in both health and disease.

	KV Channels and Vascular Tone

Top Abstract Introduction Regulation of Vascular Tone... KATP Channels and Vascular... BKCa Channels and Vascular... KV Channels and Vascular... KIR Channels and Vascular... Cl- Channels and Vascular... Store-Operated and Stretch... Summary References

 
Voltage-activated K⁺ channels, inhibited by 4-aminopyridine (also known as delayed rectifier channels), are another ubiquitous class of K⁺ channels expressed by vascular smooth muscle cells.⁷ These channels are activated by membrane depolarization with threshold potentials for substantial activation of -30 mV. Studies of small arteries and arterioles in vitro and vascular muscle cells isolated from arteries and arterioles have provided evidence that these channels may participate in the regulation of resting membrane potential and vascular tone.^{7 8 27} K_V channels may also participate in the mechanism of action of both vasodilators and vasoconstrictors^{7 68 69} : vasodilators that act via the cAMP signaling cascade may open these channels, and vasoconstrictors may close K_V channels by mechanisms that involve elevated intracellular Ca²⁺ and protein kinase C. Their role in vivo has not been explored, largely because of the lack of availability of inhibitors selective for the channels expressed in vascular muscle cells. However, electrophysiological studies indicate a decreased functional expression of K_V channels in vascular muscle cells from hypertensive animals, which may contribute to depolarization and an increase in vascular tone in this disease.⁷⁰

	KIR Channels and Vascular Tone

Top Abstract Introduction Regulation of Vascular Tone... KATP Channels and Vascular... BKCa Channels and Vascular... KV Channels and Vascular... KIR Channels and Vascular... Cl- Channels and Vascular... Store-Operated and Stretch... Summary References

 
Inward rectifier K⁺ channels were first identified by Katz in skeletal muscle⁷¹ and subsequently have been found in both excitable and nonexcitable cells (see references 31, 72, and 73 for further examples). These ion channels pass inward K⁺ current much more readily than outward current with physiological ion gradients and also show a parallel rightward shift in the potential at which rectification appears (activation potential) and a large increase in conductance with increases in the extracellular K⁺ concentration. Very little is known about the role played by K_IR channels in the regulation of resting membrane potential and tone, and data that are available are difficult to interpret. Superfusion of guinea pig submucosa in vitro with Ba²⁺ ions causes depolarization of arterioles from -70 to -40 mV.^{74 75 76} These data suggest that K_IR channels may be active under resting conditions and contribute to resting membrane potential in this preparation. The relevance of these observations to other preparations and normal physiological conditions is not known. Membrane potential in submucosal arterioles is very negative relative to what has been measured in other vascular preparations under resting, unstimulated conditions.^{7 77} It is possible that due to the conditions of the preparation (isolated, unperfused tissue with unpressurized vasculature), K_IR channels are activated. In vascular muscle cells isolated from rat ventricular septal arteries, 100 µmol/L Ba²⁺ causes a small inhibition of outward current at -50 mV, which suggests that K_IR channels may be active at resting membrane potential in these cells.⁷⁸ Despite this supporting evidence, studies of isolated, cannulated, septal arteries have failed to identify a significant role for K_IR channels in the regulation of resting membrane potential and tone.⁷⁹ Preliminary studies suggest that 50 µmol/L Ba²⁺ causes constriction of rat arterioles in cremaster muscle in vivo.⁵⁵ In contrast, studies of hamster cremasteric arteriolar muscle cells have found no effect of Ba²⁺ on currents around the resting membrane potential.²⁶ These data are inconsistent with the hypothesis that K_IR channels are active under resting conditions. Thus, the role played by K_IR channels in the regulation of resting membrane potential and tone remains unclear.

In cerebral, coronary, and skeletal muscle vascular beds, elevated extracellular K⁺, as might arise from increases in nerve or muscle activity, causes vasodilation that is associated with hyperpolarization of the vascular smooth muscle membrane.^{7 31 79 80} Two mechanisms have been proposed to explain this K⁺-induced hyperpolarization: activation of Na⁺/K⁺ ATPase and activation of K_IR channels. Early studies showed that K⁺ -induced vasodilation could be inhibited by ouabain, which suggests that Na⁺/K⁺ ATPase might be involved in this process.^{77 80} However, more recent evidence suggests that K_IR channels mediate K⁺-induced vasodilation in cerebral and coronary resistance arteries.^{7 31 79 81 82 83} Preliminary data support a role for K_IR channels in K⁺-induced dilation of arterioles in cremaster muscle.⁵⁵ However, previous studies in this preparation have shown that K⁺ induced dilation can be inhibited by millimolar concentrations of ouabain.⁸⁴ Thus, the role played by K_IR channels in K⁺-induced vasodilation of skeletal muscle arterioles remains unclear.

	Cl- Channels and Vascular Tone

Top Abstract Introduction Regulation of Vascular Tone... KATP Channels and Vascular... BKCa Channels and Vascular... KV Channels and Vascular... KIR Channels and Vascular... Cl- Channels and Vascular... Store-Operated and Stretch... Summary References

 
Chloride channels have also been proposed to regulate vascular tone.^{9 10 11} As with K⁺ ions, the electrochemical gradient for Cl^- is such that opening of Cl^- channels will result in efflux of Cl^- from vascular muscle cells (Figure 2). However, because of the negative charge, this efflux will result in depolarization and vasoconstriction (Figure 2). Closing the Cl^- channels will have the opposite effect (Figure 2). Vascular muscle cells appear to express 2 different types of chloride channels: Ca²⁺-activated Cl^- (Cl_Ca) channels⁹ and volume-regulated Cl^- (Cl_VR) channels.^{10 11} Like BK_Ca channels, Cl_Ca channels are activated by increases in intracellular Ca²⁺, and several studies have proposed that these channels are activated by vasoconstrictors and participate in the depolarization that is associated with vasoconstrictor-induced tone.⁹ However, other investigators have argued that Cl_Ca channels could have little effect on membrane potential because of the high density of BK_Ca channels and their large conductance.⁸⁵

View larger version (26K): [in this window] [in a new window]   Figure 2. Cl- channels and vascular tone. Schematic of a vascular smooth muscle cell (top) and cross sections through an arteriole (bottom) that shows that opening of Cl- channels leads to diffusion of Cl- ions out of the cell, membrane depolarization, opening of voltage-gated Ca2+ channels, increased intracellular Ca2+, etc (see text), which leads to vasoconstriction. Closure of Cl- channels has the opposite effect.

More recently, interest has been generated in Cl_VR channels. Nelson and colleagues¹⁰ demonstrated that Cl^- channel blockers dilated and hyperpolarized myogenically active cerebral arteries, which supports a role for Cl^- channels in regulation of resting membrane potential and myogenic tone. The pharmacological profile that they found was inconsistent with Cl_Ca channels, so they hypothesized that Cl_VR channels were involved. Subsequently, expression of a Cl_VR channel (ClC-3) was documented in canine pulmonary arteries,¹¹ which further supports a role for this class of ion channel in the regulation of vascular tone.

However, the picture has become considerably more cloudy. Indanyloxyacetic acid, used in the functional studies mentioned above,¹⁰ has recently been shown to block voltage-gated, dihydropyridine-sensitive Ca²⁺ channels in vascular muscle cells in the same concentration range as it inhibits tone.⁸⁶ Indanyloxyacetic acid has also been shown to activate TEA- and glibenclamide-sensitive K⁺ currents in vascular muscle cells.⁸⁷ Another chloride blocker, 5-nitro-2-(3-phenylpropylamino)benzoic acid not only blocks L-type Ca²⁺ channels,⁸⁶ but has also been demonstrated to inhibit currents through other calcium influx pathways in endothelial cells.⁸⁸ These additional effects confound simple interpretation of results obtained with Cl^- channel blockers. Thus, further research will be required to establish the role played by Cl^- channels in the regulation of vascular tone.

	Store-Operated and Stretch-Activated Ca2+ Channels and Vascular Tone

Top Abstract Introduction Regulation of Vascular Tone... KATP Channels and Vascular... BKCa Channels and Vascular... KV Channels and Vascular... KIR Channels and Vascular... Cl- Channels and Vascular... Store-Operated and Stretch... Summary References

 
Calcium not only enters vascular muscle cells through voltage-gated Ca²⁺ channels, but also through store-operated Ca²⁺ (SOC) channels^{12 13} and stretch-activated cation (SAC) channels.^{14 15 16} SOC channels are activated when intracellular calcium stores empty through an as yet not well defined signaling pathway.¹³ In other cell types, this pathway provides a means to refill the stores. Recent evidence suggests that this pathway may also be important in the regulation of vascular tone.¹² However, these ion channels have not been investigated in resistance arteries or arterioles.

Calcium may also enter vascular muscle cells through SAC channels.^{14 15 16} Studies in isolated porcine coronary muscle cells have provided evidence for SAC channels permeable to Ca²⁺ that are responsible, in part, for stretch-induced depolarization of these vascular muscle cells¹⁴ and that result in an influx of Ca²⁺ sufficient to increase intracellular Ca²⁺ even when dihydropyridine-sensitive channels are inhibited.¹⁵ Similar results were recently obtained in mesenteric resistance arteries from guinea pig.¹⁶ These data support the hypothesis that SAC channels may be involved in the regulation of myogenic tone. Their role in vivo has not been examined.

	Summary

Top Abstract Introduction Regulation of Vascular Tone... KATP Channels and Vascular... BKCa Channels and Vascular... KV Channels and Vascular... KIR Channels and Vascular... Cl- Channels and Vascular... Store-Operated and Stretch... Summary References

 
The brief outline presented above clearly demonstrates that ion channels play a central role in the regulation of vascular tone. As depicted in Figure 3, Ca²⁺ influx through voltage-gated Ca²⁺, SOC, and SAC channels provides a major source of activator Ca²⁺ used by resistance arteries and arterioles. In addition, K⁺ and Cl^- channels and the Ca²⁺ channels mentioned previously all are involved in the determination of the membrane potential of these cells (Figure 3). In turn, membrane potential, with intracellular Ca²⁺, regulates and modulates Ca²⁺ influx and Ca²⁺ release and Ca²⁺ sensitivity of the contractile machinery (Figure 3). In addition, although this is not covered in detail in the present review, functions of many of these channels are modulated by the signals and signaling pathways depicted in Figure 3. Thus, ion channels are involved to an important degree in the generation of vascular tone and in neural, humoral, and local regulation of this critical variable.

View larger version (25K): [in this window] [in a new window]   Figure 3. Ion channels and vascular tone. Schematic of a cross section through part of a vascular muscle cell. Along the top membrane are shown KIR, KATP, KV, and BKCa channels. Also shown are voltage-gated Ca2+ channels, 2 types of Cl- channels (see text), SOC channels (SOCC), and SAC channels (SACC). Shown in the membranes of the sarcoplasmic reticulum (SR) are ryanodine receptors (RyR) and inositol 1,4,5-trisphosphate receptors (IP3R). Bottom, A few of the signals that are known to modulate the function of the ion channels depicted. AC indicates adenylate cyclase; PKA, cAMP-dependent protein kinase; sGC, soluble guanylate cyclase; PKG, cGMP-dependent protein kinase; EETs, epoxyeicostetraenoic acid (epoxides of arachidonic acid; see text); PLC,phospholipase C; DAG,diacylglycerol; PKC=protein kinase C; and 20-HETE, 20-OH-arachidonic acid. See text for details.

	Acknowledgments

 
This work was supported by Public Health Service grant HL-32469.

	Footnotes

 
Received September 13, 1999; first decision October 20, 1999; revision accepted October 26, 1999.

	References

Top Abstract Introduction Regulation of Vascular Tone... KATP Channels and Vascular... BKCa Channels and Vascular... KV Channels and Vascular... KIR Channels and Vascular... Cl- Channels and Vascular... Store-Operated and Stretch... Summary References

 
1. Nelson MT, Patlak JB, Worley JF, Standen NB. Calcium channels, potassium channels, and voltage dependence of arterial smooth muscle tone. Am J Physiol Cell Physiol. 1990;259:C3–C18.[Abstract/Free Full Text]

2. Hughes AD. Calcium channels in vascular smooth muscle cells. J Vasc Res. 1995;32:353–370.[Medline] [Order article via Infotrieve]

3. Ganitkevich VY, Isenberg G. Membrane potential modulates inositol 1,4,5-trisphosphate-mediated Ca²⁺ transients in guinea-pig coronary myocytes. J Physiol (Lond). 1993;470:35–44.[Abstract/Free Full Text]

4. Yamagishi T, Yanagisawa T, Taira N. K⁺ channel openers, cromakalim and Ki4032, inhibit agonist-induced Ca²⁺ release in canine coronary artery. Naunyn Schmiedebergs Arch Pharmacol. 1992;346:691–700.[Medline] [Order article via Infotrieve]

5. Kukuljan M, Rojas E, Catt KJ, Stojilkovic SS. Membrane potential regulates inositol 1,4,5-trisphosphate-controlled cytoplasmic Ca²⁺ oscillations in pituitary gonadotrophs. J Biol Chem. 1994;269:4860–4865.[Abstract/Free Full Text]

6. Okada Y, Yanagisawa T, Taira N. BRL 38227 (levcromakalim)-induced hyperpolarization reduces the sensitivity to Ca²⁺ of contractile elements in canine coronary artery. Naunyn Schmiedebergs Arch Pharmacol. 1993;347:438–444.[Medline] [Order article via Infotrieve]

7. Nelson MT, Quayle JM. Physiological roles and properties of potassium channels in arterial smooth muscle. Am J Physiol. 1995;268:C799–C822.[Abstract/Free Full Text]

8. Jackson WF. Potassium channels and regulation of the microcirculation. Microcirculation. 1998;5:85–90.[Medline] [Order article via Infotrieve]

9. Large WA, Wang Q. Characteristics and physiological role of the Ca⁽²⁺⁾-activated Cl^- conductance in smooth muscle. Am J Physiol. 1996;271:C435–C454.[Abstract/Free Full Text]

10. Nelson MT, Conway MA, Knot HJ, Brayden JE. Chloride channel blockers inhibit myogenic tone in rat cerebral arteries. J Physiol (Lond). 1997;502:259–264.[Abstract/Free Full Text]

11. Yamazaki J, Duan D, Janiak R, Kuenzli K, Horowitz B, Hume JR. Functional and molecular expression of volume-regulated chloride channels in canine vascular smooth muscle cells [see comments]. J Physiol (Lond). 1998;507:729–736.[Abstract/Free Full Text]

12. Gibson A, McFadzean I, Wallace P, Wayman CP. Capacitative Ca²⁺ entry and the regulation of smooth muscle tone. Trends Pharmacol Sci. 1998;19:266–269.[Medline] [Order article via Infotrieve]

13. Berridge MJ. Elementary and global aspects of calcium signalling. J Physiol (Lond). 1997;499:291–306.[Free Full Text]

14. Davis MJ, Donovitz JA, Hood JD. Stretch-activated single-channel and whole cell currents in vascular smooth muscle cells. Am J Physiol Cell Physiol. 1992;262:C1083–C1088.[Abstract/Free Full Text]

15. Davis MJ, Meininger GA, Zawieja DC. Stretch-induced increases in intracellular calcium of isolated vascular smooth muscle cells. Am J Physiol Heart Circ Physiol. 1992;263:H1292–H1299.[Abstract/Free Full Text]

16. Setoguchi M, Ohya Y, Abe I, Fujishima M. Stretch-activated whole-cell currents in smooth muscle cells from mesenteric resistance artery of guinea-pig. J Physiol (Lond). 1997;501:343–353.[Abstract/Free Full Text]

17. Knot HJ, Standen NB, Nelson MT. Ryanodine receptors regulate arterial diameter and wall [Ca²⁺] in cerebral arteries of rat via Ca²⁺-dependent K⁺ channels. J Physiol (Lond). 1998;508:211–221.[Abstract/Free Full Text]

18. Boittin FX, Macrez N, Halet G, Mironneau J. Norepinephrine-induced Ca⁽²⁺⁾ waves depend on InsP₍₃₎ and ryanodine receptor activation in vascular myocytes. Am J Physiol. 1999;277:C139–C151.

19. Nilius B, Viana F, Droogmans G. Ion channels in vascular endothelium. Annu Rev Physiol. 1997;59:145–170.[Medline] [Order article via Infotrieve]

20. Lindbom L, Persson MG, Öhlén A, Borgstrm P, Gustafsson D. Effects of felodipine on microvascular resting tone and responses to nerve stimulation and perfusion pressure reduction in rabbit skeletal muscle. J Cardiovasc Pharmacol. 1990;15:592–597.[Medline] [Order article via Infotrieve]

21. Davis MJ, Hill MA. Signaling mechanisms underlying the vascular myogenic response. Physiol Rev. 1999;79:387–423.[Abstract/Free Full Text]

22. Schubert R, Mulvany MJ. The myogenic response: established facts and attractive hypotheses. Clin Sci (Colch). 1999;96:313–326.[Medline] [Order article via Infotrieve]

23. Hill MA, Meininger GA. Calcium entry and myogenic phenomena in skeletal muscle arterioles. Am J Physiol Heart Circ Physiol. 1994;267:H1085–H1092.[Abstract/Free Full Text]

24. Welsh DG, Jackson WF, Segal SS. Oxygen induces electromechanical coupling in arteriolar smooth muscle cells: a role for L-type Ca²⁺ channels. Am J Physiol. 1998;274:H2018–H2024.

25. Jackson WF, Blair KL. Characterization and function of Ca⁺⁺-activated K⁺ channels in hamster cremasteric arteriolar muscle cells. Am J Physiol Heart Circ Physiol. 1998;274:H27–H34.[Abstract/Free Full Text]

26. Jackson WF. Potassium increases barium-sensitive potassium conductance of cremasteric arteriolar muscle cells. FASEB J. 1998;12:A14. Abstract.

27. Jackson WF, Huebner JM, Rusch NJ. Enzymatic isolation and characterization of single vascular smooth muscle cells from cremasteric arterioles. Microcirculation. 1997;4:35–50.[Medline] [Order article via Infotrieve]

28. Noma A. ATP-regulated K⁺ channels in cardiac muscle. Nature. 1983;305:147–148.[Medline] [Order article via Infotrieve]

29. Babenko AP, Aguilar-Bryan L, Bryan J. A view of sur/KIR6.X, K_ATP channels. Annu Rev Physiol. 1998;60:667–687.[Medline] [Order article via Infotrieve]

30. Aguilar-Bryan L, Clement JP, Gonzalez G, Kunjilwar K, Babenko A, Bryan J. Toward understanding the assembly and structure of K_ATP channels. Physiol Rev. 1998;78:227–245.[Abstract/Free Full Text]

31. Quayle JM, Nelson MT, Standen NB. ATP-sensitive and inwardly rectifying potassium channels in smooth muscle. Physiol Rev. 1997;77:1165–1232.[Abstract/Free Full Text]

32. Ashcroft FM, Gribble FM. Correlating structure and function in ATP-sensitive K⁺ channels [In Process Citation]. Trends Neurosci. 1998;21:288–294.[Medline] [Order article via Infotrieve]

33. Jackson WF, König A, Dambacher T, Busse R. Prostacyclin-induced vasodilation in the rabbit heart is mediated by ATP-sensitive potassium channels. Am J Physiol Heart Circ Physiol. 1993;264:H238–H243.[Abstract/Free Full Text]

34. Jackson WF. Arteriolar tone is determined by activity of ATP-sensitive potassium channels. Am J Physiol Heart Circ Physiol. 1993;265:H1797–H1803.[Abstract/Free Full Text]

35. Saito Y, McKay M, Eraslan A, Hester RL. Functional hyperemia in striated muscle is reduced following blockade of ATP-sensitive potassium channels. Am J Physiol Heart Circ Physiol. 1996;270(pt 2):H1649–H1654.

36. Tateishi J, Faber JE. ATP-sensitive K⁺ channels mediate alpha_2D-adrenergic receptor contraction of arteriolar smooth muscle and reversal of contraction by hypoxia. Circ Res. 1995;76:53–63.[Abstract/Free Full Text]

37. Vanelli G, Hussain SN. Effects of potassium channel blockers on basal vascular tone and reactive hyperemia of canine diaphragm. Am J Physiol. 1994;266:H43–H51.[Abstract/Free Full Text]

38. Kosmas EN, Levy RD, Hussain SN. Acute effects of glyburide on the regulation of peripheral blood flow in normal humans. Eur J Pharmacol. 1995;274:193–199.[Medline] [Order article via Infotrieve]

39. Vanelli G, Chang HY, Gatensby AG, Hussain SNA. Contribution of potassium channels to active hyperemia of the canine diaphragm. J Appl Physiol. 1994;76:1098–1105.[Abstract/Free Full Text]

40. Thomas GD, Hansen J, Victor RG. ATP-sensitive potassium channels mediate contraction-induced attenuation of sympathetic vasoconstriction in rat skeletal muscle. J Clin Invest. 1997;99:2602–2609.[Medline] [Order article via Infotrieve]

41. Banitt PF, Smits P, Williams SB, Ganz P, Creager MA. Activation of ATP-sensitive potassium channels contributes to reactive hyperemia in humans. Am J Physiol. 1996;271:H1594–H1598.[Abstract/Free Full Text]

42. Minkes RK, Santiago JA, McMahon TJ, Kadowitz PJ. Role of K⁺_ATP channels and EDRF in reactive hyperemia in the hindquarters vascular bed of cats. Am J Physiol. 1995;269:H1704–H1712.[Abstract/Free Full Text]

43. Vallet B, Curtis SE, Guery B, Mangalaboyi J, Menager P, Cain SM, Chopin C, Dupuis BA. ATP-sensitive K⁺ channel blockade impairs O₂ extraction during progressive ischemia in pig hindlimb. J Appl Physiol. 1995;79:2035–2042.[Abstract/Free Full Text]

44. Smith MP, Humphrey SJ, Jackson WF. Selective in vivo antagonism of pinacidil-induced hypotension by the guanidine U37883A in anesthetized rats. Pharmacology. 1994;49:363–375.[Medline] [Order article via Infotrieve]

45. Mayhan WG, Faraci FM. Responses of cerebral arterioles in diabetic rats to activation of ATP-sensitive potassium channels. Am J Physiol Heart Circ Physiol. 1993;265:H152–H157.[Abstract/Free Full Text]

46. Mayhan WG. Effect of diabetes mellitus on response of the basilar artery to activation of ATP-sensitive potassium channels. Brain Res. 1994;636:35–39.[Medline] [Order article via Infotrieve]

47. Zimmermann PA, Knot HJ, Stevenson AS, Nelson MT. Increased myogenic tone and diminished responsiveness to ATP-sensitive K⁺ channel openers in cerebral arteries from diabetic rats. Circ Res. 1997;81:996–1004.[Abstract/Free Full Text]

48. Crijns FR, Struijker Boudier HA, Wolffenbuttel BH. Arteriolar reactivity in conscious diabetic rats: influence of aminoguanidine treatment. Diabetes. 1998;47:918–923.[Abstract]

49. Hille B. Ionic Channels of Excitable Membranes. 2^nd ed. Sunderland, Mass: Sinauer Associates, Inc; 1992:115–139.

50. Carl A, Lee HK, Sanders KM. Regulation of ion channels in smooth muscles by calcium. Am J Physiol. 1996;271:C9–C34.[Abstract/Free Full Text]

51. Nelson MT, Cheng H, Rubart M, Santana LF, Bonev AD, Knot HJ, Lederer WJ. Relaxation of arterial smooth muscle by calcium sparks [Published comment: Science.. 1995;270:588–589]. Science. 1995;270:633–637.[Abstract/Free Full Text]

52. Brayden JE, Nelson MT. Regulation of arterial tone by activation of calcium-dependent potassium channels. Science. 1992;256:532–535.[Abstract/Free Full Text]

53. Jaggar JH, Wellman GC, Heppner TJ, Porter VA, Perez GJ, Gollasch M, Kleppisch T, Rubart M, Stevenson AS, Lederer WJ, Knot HJ, Bonev AD, Nelson MT. Ca²⁺ channels, ryanodine receptors and Ca⁽²⁺⁾-activated K⁺ channels: a functional unit for regulating arterial tone. Acta Physiol Scand. 1998;164:577–587.[Medline] [Order article via Infotrieve]

54. Paterno R, Faraci FM, Heistad DD. Role of Ca⁽²⁺⁾-dependent K⁺ channels in cerebral vasodilatation induced by increases in cyclic GMP and cyclic AMP in the rat. Stroke. 1996;27:1603–1607.[Abstract/Free Full Text]

55. Loeb AL, Gdény I, Longnecker DE. Functional evidence for inward-rectifier potassium channels in rat cremaster muscle arterioles in vivo. Microcirculation. 1997;4:160. Abstract.

56. Campbell WB, Gebremedhin D, Pratt PF, Harder DR. Identification of epoxyeicosatrienoic acids as endothelium-derived hyperpolarizing factors. Circ Res. 1996;78:415–423.[Abstract/Free Full Text]

57. Wang R, Wang Z, Wu L. Carbon monoxide-induced vasorelaxation and the underlying mechanisms. Br J Pharmacol. 1997;121:927–934.[Medline] [Order article via Infotrieve]

58. Wang R, Wu L. The chemical modification of K_Ca channels by carbon monoxide in vascular smooth muscle cells. J Biol Chem. 1997;272:8222–8226.[Abstract/Free Full Text]

59. Wang R, Wu L, Wang Z. The direct effect of carbon monoxide on K_Ca channels in vascular smooth muscle cells. Pflugers Arch. 1997;434:285–291.[Medline] [Order article via Infotrieve]

60. Lange A, Gebremedhin D, Narayanan J, Harder D. 20-Hydroxyeicosatetraenoic acid-induced vasoconstriction and inhibition of potassium current in cerebral vascular smooth muscle is dependent on activation of protein kinase C. J Biol Chem. 1997;272:27345–27352.[Abstract/Free Full Text]

61. Porter VA, Bonev AD, Knot HJ, Heppner TJ, Stevenson AS, Kleppisch T, Lederer WJ, Nelson MT. Frequency modulation of Ca²⁺ sparks is involved in regulation of arterial diameter by cyclic nucleotides. Am J Physiol. 1998;274:C1346–C1355.[Abstract/Free Full Text]

62. Jaggar JH, Stevenson AS, Nelson MT. Voltage dependence of Ca²⁺ sparks in intact cerebral arteries. Am J Physiol. 1998;274:C1755–C1761.[Abstract/Free Full Text]

63. Rusch NJ, De Lucena RG, Wooldridge TA, England SK, Cowley AW Jr. A Ca²⁺-dependent K⁺ current is enhanced in arterial membranes of hypertensive rats. Hypertension. 1992;19:301–307.[Abstract/Free Full Text]

64. Asano M, Masuzawa-Ito K, Matsuda T. Charybdotoxin-sensitive K⁺ channels regulate the myogenic tone in the resting state of arteries from spontaneously hypertensive rats. Br J Pharmacol. 1993;108:214–222.[Medline] [Order article via Infotrieve]

65. Asano M, Matsuda T, Hayakawa M, Ito KM, Ito K. Increased resting Ca²⁺ maintains the myogenic tone and activates K⁺ channels in arteries from young spontaneously hypertensive rats. Eur J Pharmacol Mol Pharmacol. 1993;247:295–304.[Medline] [Order article via Infotrieve]

66. Liu Y, Pleyte K, Knaus HG, Rusch NJ. Increased expression of Ca²⁺-sensitive K⁺ channels in aorta of hypertensive rats. Hypertension. 1997;30:1403–1409.[Abstract/Free Full Text]

67. Rusch NJ, Liu Y. Potassium channels in hypertension: homeostatic pathways to buffer arterial contraction. J Lab Clin Med. 1997;130:245–251.[Medline] [Order article via Infotrieve]

68. Aiello EA, Malcolm AT, Walsh MP, Cole WC. ß-Adrenoceptor activation and PKA regulate delayed rectifier K⁺ channels of vascular smooth muscle cells. Am J Physiol.. 1998;275:H448–H459.[Abstract/Free Full Text]

69. Aiello EA, Walsh MP, Cole WC. Phosphorylation by protein kinase A enhances delayed rectifier K⁺ current in rabbit vascular smooth muscle cells. Am J Physiol Heart Circ Physiol. 1995;268:H926–H934.[Abstract/Free Full Text]

70. Martens JR, Gelband CH. Alterations in rat interlobar artery membrane potential and K⁺ channels in genetic and nongenetic hypertension. Circ Res. 1996;79:295–301.[Abstract/Free Full Text]

71. Katz B. Les constantes électriques de la membrane du muscle. Arch Sci Physiol. 1949;2:285–299.

72. Jan LY, Jan YN. Voltage-gated and inwardly rectifying potassium channels. J Physiol (Lond). 1997;505:267–282.[Abstract/Free Full Text]

73. Nichols CG, Lopatin AN. Inward rectifier potassium channels. Annu Rev Physiol. 1997;59:171–191.[Medline] [Order article via Infotrieve]

74. Hirst GDS, Edwards FR. Sympathetic neuroeffector transmission in arteries and arterioles. Physiol Rev. 1989;69(2):546–604.

75. Edwards FR, Hirst GDS. Inward rectification in submucosal arterioles of guinea-pig ileum. J Physiol (Lond). 1986;404:437–454.[Abstract/Free Full Text]

76. Hashitani H, Suzuki H. K⁺ channels which contribute to the acetylcholine-induced hyperpolarization in smooth muscle of the guinea-pig submucosal arteriole. J Physiol (Lond). 1997;501:319–329.[Abstract/Free Full Text]

77. Johansson B, Somlyo AP. Electrophysiology and excitation-contraction coupling. In: Bohr DF, Somlyo AP, Sparks HV, eds. Handbook of Physiology, Section 2: The Cardiovascular System: Vol II, Vascular Smooth Muscle. Bethesda, Md: American Physiological Society; 1980:301–323.

78. Robertson BE, Bonev AD, Nelson MT. Inward rectifier K⁺ currents in smooth muscle cells from rat coronary arteries: block by Mg,²⁺ Ca²⁺, and Ba.²⁺ Am J Physiol. 1996;271:H696–H705.[Abstract/Free Full Text]

79. Knot HJ, Zimmermann PA, Nelson MT. Extracellular K⁽⁺⁾-induced hyperpolarizations and dilatations of rat coronary and cerebral arteries involve inward rectifier K⁽⁺⁾ channels. J Physiol (Lond). 1996;492:419–430.[Abstract/Free Full Text]

80. Sparks HV. Effect of local metabolic factors on vascular smooth muscle. In: Bohr DF, Somlyo AP, Sparks HV, eds. Handbook of Physiology, Section 2: The Cardiovascular System. Bethesda, Md: American Physiological Society; 1980;181–309. Microcirculation, Part 2; vol II.

81. Edwards FR, Hirst GDS, Silverberg GD. Inward rectification in rat cerebral arterioles; involvement of potassium ions in autoregulation. J Physiol (Lond). 1988;404:455–466.[Abstract/Free Full Text]

82. Salter KJ, Kozlowski RZ. Differential electrophysiological actions of endothelin-1 on Cl^- and K⁺ currents in myocytes isolated from aorta, basilar and pulmonary artery. J Pharmacol Exp Ther. 1998;284:1122–1131.[Abstract/Free Full Text]

83. Quayle JM, McCarron JG, Brayden JE, Nelson MT. Inward rectifier K⁺ currents in smooth muscle cells from rat resistance-sized cerebral arteries. Am J Physiol Cell Physiol. 1993;265:C1363–C1370.[Abstract/Free Full Text]

84. Lombard JH, Stekiel WJ. Responses of cremasteric arterioles of spontaneously hypertensive rats to changes in extracellular K⁺ concentration. Microcirculation. 1995;2:355–362.[Medline] [Order article via Infotrieve]

85. Nelson MT. Bayliss, myogenic tone and volume-regulated chloride channels in arterial smooth muscle. J Physiol (Lond). 1998;507:629. Comment.[Free Full Text]

86. Doughty JM, Miller AL, Langton PD. Non-specificity of chloride channel blockers in rat cerebral arteries: block of the L-type calcium channel. J Physiol (Lond). 1998;507:433–439.[Abstract/Free Full Text]

87. Toma C, Greenwood IA, Helliwell RM, Large WA. Activation of potassium currents by inhibitors of calcium-activated chloride conductance in rabbit portal vein smooth muscle cells [published erratum appears in Br J Pharmacol.. 1996;119:184]. Br J Pharmacol. 1996;118:513–520.

88. Gericke M, Oike M, Droogmans G, Nilius B. Inhibition of capacitative Ca²⁺ entry by a Cl^- channel blocker in human endothelial cells. Eur J Pharmacol Mol Pharmacol. 1994;269:381–384.[Medline] [Order article via Infotrieve]

This article has been cited by other articles:

				R. D. Rainbow, R. I. Norman, D. E. Everitt, J. L. Brignell, N. W. Davies, and N. B. Standen Endothelin-I and angiotensin II inhibit arterial voltage-gated K+ channels through different protein kinase C isoenzymes Cardiovasc Res, August 1, 2009; 83(3): 493 - 500. [Abstract] [Full Text] [PDF]

				P. Chan, I-M. Liu, Y.-X. Li, W.-J. Yu, and J.-T. Cheng Antihypertension Induced by Tanshinone IIA Isolated from the Roots of Salvia Miltiorrhiza Evid. Based Complement. Altern. Med., June 19, 2009; (2009) nep056v1. [Abstract] [Full Text] [PDF]

				A. Moreno-Dominguez, P. Cidad, E. Miguel-Velado, J. R. Lopez-Lopez, and M. T. Perez-Garcia De novo expression of Kv6.3 contributes to changes in vascular smooth muscle cell excitability in a hypertensive mice strain J. Physiol., February 1, 2009; 587(3): 625 - 640. [Abstract] [Full Text] [PDF]

				M. K. McGahon, M. A. Needham, C. N. Scholfield, J. G. McGeown, and T. M. Curtis Ca2+-Activated Cl- Current in Retinal Arteriolar Smooth Muscle Invest. Ophthalmol. Vis. Sci., January 1, 2009; 50(1): 364 - 371. [Abstract] [Full Text] [PDF]

				C. P. Nelson, J. M. Willets, N. W. Davies, R. A. J. Challiss, and N. B. Standen Visualizing the temporal effects of vasoconstrictors on PKC translocation and Ca2+ signaling in single resistance arterial smooth muscle cells Am J Physiol Cell Physiol, December 1, 2008; 295(6): C1590 - C1601. [Abstract] [Full Text] [PDF]

				X.-C. Ru, L.-B. Qian, Q. Gao, Y.-F. Li, I. C. Bruce, and Q. Xia Alcohol Induces Relaxation of Rat Thoracic Aorta and Mesenteric Arterial Bed Alcohol Alcohol., September 1, 2008; 43(5): 537 - 543. [Abstract] [Full Text] [PDF]

				J. Jiao, V. Garg, B. Yang, T. S. Elton, and K. Hu Protein Kinase C-{epsilon} Induces Caveolin-Dependent Internalization of Vascular Adenosine 5'-Triphosphate-Sensitive K+ Channels Hypertension, September 1, 2008; 52(3): 499 - 506. [Abstract] [Full Text] [PDF]

				G. M. Dick, I. N. Bratz, L. Borbouse, G. A. Payne, U. D. Dincer, J. D. Knudson, P. A. Rogers, and J. D. Tune Voltage-dependent K+ channels regulate the duration of reactive hyperemia in the canine coronary circulation Am J Physiol Heart Circ Physiol, May 1, 2008; 294(5): H2371 - H2381. [Abstract] [Full Text] [PDF]

				T. Smani, A. Dominguez-Rodriguez, A. Hmadcha, E. Calderon-Sanchez, A. Horrillo-Ledesma, and A. Ordonez Role of Ca2+-Independent Phospholipase A2 and Store-Operated Pathway in Urocortin-Induced Vasodilatation of Rat Coronary Artery Circ. Res., November 26, 2007; 101(11): 1194 - 1203. [Abstract] [Full Text] [PDF]

				J.-H. Xue, L.-F. Zhang, J. Ma, and M.-J. Xie Differential regulation of L-type Ca2+ channels in cerebral and mesenteric arteries after simulated microgravity in rats and its intervention by standing Am J Physiol Heart Circ Physiol, July 1, 2007; 293(1): H691 - H701. [Abstract] [Full Text] [PDF]

				M. K. McGahon, D. P. Dash, A. Arora, N. Wall, J. Dawicki, D. A. Simpson, C. N. Scholfield, J. G. McGeown, and T. M. Curtis Diabetes Downregulates Large-Conductance Ca2+-Activated Potassium {beta}1 Channel Subunit in Retinal Arteriolar Smooth Muscle Circ. Res., March 16, 2007; 100(5): 703 - 711. [Abstract] [Full Text] [PDF]

				L. I. Brueggemann, C. J. Moran, J. A. Barakat, J. Z. Yeh, L. L. Cribbs, and K. L. Byron Vasopressin stimulates action potential firing by protein kinase C-dependent inhibition of KCNQ5 in A7r5 rat aortic smooth muscle cells Am J Physiol Heart Circ Physiol, March 1, 2007; 292(3): H1352 - H1363. [Abstract] [Full Text] [PDF]

				L. Magnusson, C. M. Sorensen, T. H. Braunstein, N.-H. Holstein-Rathlou, and M. Salomonsson Renovascular BKCa channels are not activated in vivo under resting conditions and during agonist stimulation Am J Physiol Regulatory Integrative Comp Physiol, January 1, 2007; 292(1): R345 - R353. [Abstract] [Full Text] [PDF]

				J. B. Samora, J. C. Frisbee, and M. A. Boegehold Growth-dependent changes in endothelial factors regulating arteriolar tone Am J Physiol Heart Circ Physiol, January 1, 2007; 292(1): H207 - H214. [Abstract] [Full Text] [PDF]

				I. Semenov, B. Wang, J. T. Herlihy, and R. Brenner BK channel beta1-subunit regulation of calcium handling and constriction in tracheal smooth muscle Am J Physiol Lung Cell Mol Physiol, October 1, 2006; 291(4): L802 - L810. [Abstract] [Full Text] [PDF]

				M. Wareing, S. L. Greenwood, G. K. Fyfe, and P. N. Baker Reactivity of Human Placental Chorionic Plate Vessels from Pregnancies Complicated by Intrauterine Growth Restriction (IUGR) Biol Reprod, October 1, 2006; 75(4): 518 - 523. [Abstract] [Full Text] [PDF]

				C. S. Packer Soluble guanylate cyclase (sGC) down-regulation by abnormal extracellular matrix proteins as a novel mechanism in vascular dysfunction: Implications in metabolic syndrome Cardiovasc Res, February 1, 2006; 69(2): 302 - 303. [Full Text] [PDF]

				T. Godfraind Antioxidant effects and the therapeutic mode of action of calcium channel blockers in hypertension and atherosclerosis Phil Trans R Soc B, December 29, 2005; 360(1464): 2259 - 2272. [Abstract] [Full Text] [PDF]

				E. Miguel-Velado, A. Moreno-Dominguez, O. Colinas, P. Cidad, M. Heras, M. T. Perez-Garcia, and J. R. Lopez-Lopez Contribution of Kv Channels to Phenotypic Remodeling of Human Uterine Artery Smooth Muscle Cells Circ. Res., December 9, 2005; 97(12): 1280 - 1287. [Abstract] [Full Text] [PDF]

				C. Cao, W. Lee-Kwon, E. P. Silldorff, and T. L. Pallone KATP channel conductance of descending vasa recta pericytes Am J Physiol Renal Physiol, December 1, 2005; 289(6): F1235 - F1245. [Abstract] [Full Text] [PDF]

				R. Robert, C. Norez, and F. Becq Disruption of CFTR chloride channel alters mechanical properties and cAMP-dependent Cl- transport of mouse aortic smooth muscle cells J. Physiol., October 15, 2005; 568(2): 483 - 495. [Abstract] [Full Text] [PDF]

				M.-J. Xie, L.-F. Zhang, J. Ma, and H.-W. Cheng Functional alterations in cerebrovascular K+ and Ca2+ channels are comparable between simulated microgravity rat and SHR Am J Physiol Heart Circ Physiol, September 1, 2005; 289(3): H1265 - H1276. [Abstract] [Full Text] [PDF]

				I. N. Bratz, G. M. Dick, L. D. Partridge, and N. L. Kanagy Reduced molecular expression of K+ channel proteins in vascular smooth muscle from rats made hypertensive with N{omega}-nitro-L-arginine Am J Physiol Heart Circ Physiol, September 1, 2005; 289(3): H1277 - H1283. [Abstract] [Full Text] [PDF]

				I. N. Bratz, A. N. Swafford Jr., N. L. Kanagy, and G. M. Dick Reduced functional expression of K+ channels in vascular smooth muscle cells from rats made hypertensive with N{omega}-nitro-L-arginine Am J Physiol Heart Circ Physiol, September 1, 2005; 289(3): H1284 - H1290. [Abstract] [Full Text] [PDF]

				J. Navarro-Antolin, K. L. Levitsky, E. Calderon, A. Ordonez, and J. Lopez-Barneo Decreased Expression of Maxi-K+ Channel {beta}1-Subunit and Altered Vasoregulation in Hypoxia Circulation, August 30, 2005; 112(9): 1309 - 1315. [Abstract] [Full Text] [PDF]

				M. E. Loewen and G. W. Forsyth Structure and Function of CLCA Proteins Physiol Rev, July 1, 2005; 85(3): 1061 - 1092. [Abstract] [Full Text] [PDF]

				A. M. Brainard, A. J. Miller, J. R. Martens, and S. K. England Maxi-K channels localize to caveolae in human myometrium: a role for an actin-channel-caveolin complex in the regulation of myometrial smooth muscle K+ current Am J Physiol Cell Physiol, July 1, 2005; 289(1): C49 - C57. [Abstract] [Full Text] [PDF]

				K. Boussery, C. Delaey, and J. Van de Voorde The Vasorelaxing Effect of CGRP and Natriuretic Peptides in Isolated Bovine Retinal Arteries Invest. Ophthalmol. Vis. Sci., April 1, 2005; 46(4): 1420 - 1427. [Abstract] [Full Text] [PDF]

				S. J Haug and S. S Segal Sympathetic neural inhibition of conducted vasodilatation along hamster feed arteries: complementary effects of {alpha}1- and {alpha}2-adrenoreceptor activation J. Physiol., March 1, 2005; 563(2): 541 - 555. [Abstract] [Full Text] [PDF]

				T. Suzuki and K. Takimoto Differential expression of Kv4 pore-forming and KChIP auxiliary subunits in rat uterus during pregnancy Am J Physiol Endocrinol Metab, February 1, 2005; 288(2): E335 - E341. [Abstract] [Full Text] [PDF]

				T. L. Pallone, C. Cao, and Z. Zhang Inhibition of K+ conductance in descending vasa recta pericytes by ANG II Am J Physiol Renal Physiol, December 1, 2004; 287(6): F1213 - F1222. [Abstract] [Full Text] [PDF]

				Z.-J. Fu, M.-J. Xie, L.-F. Zhang, H.-W. Cheng, and J. Ma Differential activation of potassium channels in cerebral and hindquarter arteries of rats during simulated microgravity Am J Physiol Heart Circ Physiol, October 1, 2004; 287(4): H1505 - H1515. [Abstract] [Full Text] [PDF]

				G. D. Thomas and S. S. Segal Neural control of muscle blood flow during exercise J Appl Physiol, August 1, 2004; 97(2): 731 - 738. [Abstract] [Full Text] [PDF]

				J.-I. Kaide, F. Zhang, Y. Wei, W. Wang, V. R. Gopal, J. R. Falck, M. Laniado-Schwartzman, and A. Nasjletti Vascular CO Counterbalances the Sensitizing Influence of 20-HETE on Agonist-Induced Vasoconstriction Hypertension, August 1, 2004; 44(2): 210 - 216. [Abstract] [Full Text] [PDF]

				P. S. Clifford and Y. Hellsten Vasodilatory mechanisms in contracting skeletal muscle J Appl Physiol, July 1, 2004; 97(1): 393 - 403. [Abstract] [Full Text] [PDF]

				R. Robert, V. Thoreau, C. Norez, A. Cantereau, A. Kitzis, Y. Mettey, C. Rogier, and F. Becq Regulation of the Cystic Fibrosis Transmembrane Conductance Regulator Channel by {beta}-Adrenergic Agonists and Vasoactive Intestinal Peptide in Rat Smooth Muscle Cells and Its Role in Vasorelaxation J. Biol. Chem., May 14, 2004; 279(20): 21160 - 21168. [Abstract] [Full Text] [PDF]

				J. Steendahl, N.-H. Holstein-Rathlou, C. M. Sorensen, and M. Salomonsson Effects of chloride channel blockers on rat renal vascular responses to angiotensin II and norepinephrine Am J Physiol Renal Physiol, February 1, 2004; 286(2): F323 - F330. [Abstract] [Full Text] [PDF]

				K. Rhinehart, C. A. Handelsman, E. P. Silldorff, and T. L. Pallone ANG II AT2 receptor modulates AT1 receptor-mediated descending vasa recta endothelial Ca2+ signaling Am J Physiol Heart Circ Physiol, March 1, 2003; 284(3): H779 - H789. [Abstract] [Full Text] [PDF]

				B. Adegunloye, E. Lamarre, and R. S. Moreland Quinine Inhibits Vascular Contraction Independent of Effects on Calcium or Myosin Phosphorylation J. Pharmacol. Exp. Ther., January 1, 2003; 304(1): 294 - 300. [Abstract] [Full Text] [PDF]

				K. Rhinehart, Z. Zhang, and T. L. Pallone Ca2+ signaling and membrane potential in descending vasa recta pericytes and endothelia Am J Physiol Renal Physiol, October 1, 2002; 283(4): F852 - F860. [Abstract] [Full Text] [PDF]

				E. A. Coppock and M. M. Tamkun Differential expression of KV channel alpha - and beta -subunits in the bovine pulmonary arterial circulation Am J Physiol Lung Cell Mol Physiol, December 1, 2001; 281(6): L1350 - L1360. [Abstract] [Full Text] [PDF]

				A. W. Miller, C. Dimitropoulou, G. Han, R. E. White, D. W. Busija, and G. O. Carrier Epoxyeicosatrienoic acid-induced relaxation is impaired in insulin resistance Am J Physiol Heart Circ Physiol, October 1, 2001; 281(4): H1524 - H1531. [Abstract] [Full Text] [PDF]

				D. W. Landry and J. A. Oliver The Pathogenesis of Vasodilatory Shock N. Engl. J. Med., August 23, 2001; 345(8): 588 - 595. [Full Text] [PDF]

				M. A. Hill, H. Zou, S. J. Potocnik, G. A. Meininger, and M. J. Davis Signal Transduction in Smooth Muscle: Invited Review: Arteriolar smooth muscle mechanotransduction: Ca2+ signaling pathways underlying myogenic reactivity J Appl Physiol, August 1, 2001; 91(2): 973 - 983. [Abstract] [Full Text] [PDF]

				B. Li, C. L. Chik, A. K. Ho, and E. Karpinski L-Type Ca2+ Channel Regulation by Pituitary Adenylate Cyclase-Activating Polypeptide in Vascular Myocytes from Spontaneously Hypertensive Rats Endocrinology, July 1, 2001; 142(7): 2865 - 2873. [Abstract] [Full Text] [PDF]

				E. A. Coppock, J. R. Martens, and M. M. Tamkun Molecular basis of hypoxia-induced pulmonary vasoconstriction: role of voltage-gated K+ channels Am J Physiol Lung Cell Mol Physiol, July 1, 2001; 281(1): L1 - L12. [Abstract] [Full Text] [PDF]

				F. Zhang, J.-I. Kaide, Y. Wei, H. Jiang, C. Yu, M. Balazy, N. G. Abraham, W. Wang, and A. Nasjletti Carbon monoxide produced by isolated arterioles attenuates pressure-induced vasoconstriction Am J Physiol Heart Circ Physiol, July 1, 2001; 281(1): H350 - H358. [Abstract] [Full Text] [PDF]

				M.Y. Alexander Chloride ions and the endothelium: their role in adrenoceptor-mediated vasoconstriction Cardiovasc Res, December 1, 2000; 48(3): 365 - 366. [Full Text] [PDF]

				A. J. Wilson, R. I. Jabr, and L. H. Clapp Calcium Modulation of Vascular Smooth Muscle ATP-Sensitive K+ Channels : Role of Protein Phosphatase-2B Circ. Res., November 24, 2000; 87(11): 1019 - 1025. [Abstract] [Full Text] [PDF]

This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Jackson, W. F. Search for Related Content PubMed PubMed Citation Articles by Jackson, W. F. Related Collections Calcium cycling/excitation-contraction coupling Cell signalling/signal transduction Hypertension - basic studies Ion channels/membrane transport