(Hypertension. 1998;32:1060-1065.)
© 1998 American Heart Association, Inc.
Scientific Contributions |
Biophysical Signals Underlying Myogenic Responses in Rat Interlobular Artery
Presented in part at the 52nd Annual Fall Conference and Scientific Sessions of the Council for High Blood Pressure Research, Philadelphia, Pa, September 15–18, 1998, and published in abstract form (Hypertension. 1998;32:616.).
From the Department of Medicine, Saitama Medical School, Iruma, Saitama (T.T., H.S., H.O.), and Department of Medicine, School of Medicine, Keio University, Shinjuku, Tokyo (K.H., Y.O., T.S.), Japan.
Correspondence to Takao Saruta, MD, Department of Medicine, School of Medicine, Keio University, 35 Shinanomachi, Shinjuku, Tokyo 160-8582, Japan.
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Abstract |
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Abstract—To assess cellular mechanisms mediating myogenic responses of interlobular artery (ILA), experiments were performed with the use of isolated perfused hydronephrotic kidneys. ILAs were divided into 3 groups according to their basal diameters: proximal (>60 µm), intermediate (40 to 60 µm), and distal (<40 µm) ILAs. Myogenic responses were obtained by stepwise increase in perfusion pressure. Greater myogenic responsiveness was observed in ILAs with smaller diameters. Diltiazem (10 µmol/L) inhibited myogenic responses of all segments of ILAs. Furthermore, gadolinium (10 µmol/L), a mechanosensitive cation channel blocker, abolished myogenic responses of distal but not proximal ILA. In contrast, 2-nitro-4-carboxyphenyl-N, N-diphenyl-carbamate (200 µmol/L), an inhibitor of phospholipase C, prevented myogenic responses of proximal but not distal ILA. Finally, basal proximal ILA diameters were increased by treatment with 50 nmol/L of staurosporine (P<0.05), and subsequent addition of thapsigargin (1 µmol/L) blocked myogenic contraction of proximal ILAs. Myogenic responses of intermediate ILAs exhibited characteristics between those of distal and proximal ILAs. Our data indicate that underlying mechanisms for myogenic responses differ in distinct segments of ILAs. The present results suggest that mechanosensitive cation channels are involved in myogenic constriction of distal ILAs. Finally, our findings provide evidence that the stimulation of phospholipase C mediates myogenic contraction of proximal ILAs.
Key Words: phospholipases • calcium • protein kinase C • membrane potential • calcium channels
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Introduction |
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An elevation of transmural pressure elicits the increase in tension of vessel wall.1 Numerous studies have indicated that this myogenic response plays an important role in regulation of capillary blood flow and pressure. There is still inconsistency regarding the mechanisms mediating myogenic responses. On the one hand, previous studies demonstrated that increasing pressure stimulates phospholipase C, thereby mobilizing intracellular calcium and mediating arterial myogenic response.2 On the other hand, arteriolar myogenic constriction depends on extracellular calcium.3
Kidneys exhibit remarkable capacity to maintain constant blood flow despite marked variations in blood pressure.4 Recent results indicate that renal autoregulatory capacity was diminished in various pathophysiological conditions, including hypertension, diabetes mellitus, and progressive renal diseases.5 6 7 Furthermore, deranged renal autoregulation allows direct transmission of systemic blood pressure to glomeruli, thereby further worsening renal injury.7 Thus, the elucidation of mechanisms mediating autoregulation would be of great interest and could provide a theoretical framework for developing therapeutic strategies against chronic renal diseases. Carmines et al8 demonstrated that increasing pressure constricted all segments of preglomerular vessels, including afferent arteriole, interlobular artery (ILA), and arcuate artery. In addition to tubuloglomerular feedback (TGF), intact myogenic constriction is required for efficient autoregulation of glomerular blood flow.9 The afferent arteriole, which is the target of TGF, plays the most important role in autoregulatory adjustments of renal vascular resistance,8 but myogenic responses of ILAs also substantively participate in total renal autoregulation.10 11 While recent studies have validated that endothelium is not required for pressure-induced renal vasoconstriction,4 12 there is a paucity of data regarding mechanisms mediating myogenic response of ILAs.
In the present study experiments were performed with the use of isolated perfused hydronephrotic kidney model devoid of complex interactions between TGF and myogenic response.13 14 The effects of gadolinium, a potent mechanosensitive cation channel blocker,3 15 and 2-nitro-4-carboxyphenyl-N, N-diphenyl-carbamate (NCDC), an inhibitor of phospholipase C,2 16 were assessed. The present results indicate that myogenic responses are mediated by differing mechanisms in distinct segments of ILAs. Our data indicate that NCDC blocked myogenic response of proximal ILAs, providing evidence that myogenic response in proximal ILAs is mediated by the stimulation of phospholipase C. Our findings that myogenic constriction of distal ILAs was inhibited by either gadolinium or diltiazem suggest that pressure gates mechanosensitive cation channels, thereby activating voltage-dependent calcium channels in distal ILAs.
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Methods |
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Gadolinium was purchased from Aldrich. Diltiazem and NCDC were obtained from Sigma. Thapsigargin and staurosporine were obtained from Research Biochemical.
Experiments were performed as described
previously.3 16 In brief, hydronephrosis was
induced in 19 adult male Sprague-Dawley rats (Charles River Japan,
Atsugi, Kanagawa) by ligating the right ureter under ether
anesthesia. Eight to 10 weeks after the surgery, when renal
tubular atrophy had progressed to a stage that allowed direct
microscopic visualization of myogenic responses along the entire length
of intact ILAs (Figure 1
), the right
kidney was harvested for perfusion study. ILA diameters were estimated
with an automated program custom designed to determine the mean
distance between parallel vessel walls.17 Three
separate segments, 
10 to 50 µm in length, were chosen from an
ILA. As described previously,18 the segments of
ILAs were divided into 3 groups according to their basal diameters at
80 mm Hg: proximal(>60 µm), intermediate (40 to 60
µm), and distal (<40 µm) ILAs.
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In the first series of experiments (5 kidneys), initially basal myogenic responses were observed. Subsequently, diltiazem was added to achieve a final concentration of 10 µmol/L.14 Pressure challenge was again performed. Finally, potassium concentration in the perfusate was isosmotically increased to 30 mmol/L.5
In the second series of studies, the kidneys (n=5) were exposed to 10 µmol/L of gadolinium after basal myogenic responses were assessed.3 In the presence of gadolinium, pressure challenge was performed, after which NCDC (200 µmol/L) was added.16 Thirty minutes later, myogenic responses were assessed. Finally, the responses to high-potassium media were examined.
Direct effects of NCDC on myogenic responses were examined in the third group (4 kidneys). Basal myogenic responses were assessed, then NCDC (200 µmol/L) was added directly to the perfusate. Finally, pressure challenge was performed. This concentration of NCDC was selected because it abolished Al/NaF-induced renal vasoconstriction under our experimental conditions.16
In the fourth studies (5 kidneys), basal myogenic responses were examined, then 50 nmol/L of staurosporine was added.19 Thirty minutes later, pressure challenge was performed. Subsequently, thapsigargin (1 µmol/L) was added. After 30 minutes of reequilibration periods, myogenic responses were again assessed.16 Finally, high-potassium medium was added. Previous results suggest that in our experimental model, staurosporine (50 nmol/L) and thapsigargin (1 µmol/L) blocked the activation of protein kinase C and calcium mobilization, respectively.
All experimental procedures were approved by our institutional ethical committees. Data were expressed as mean±SE. Statistical significance was examined by linear regression analysis, Student's t test, and ANOVA followed by the Newman-Keuls test. P<0.05 was considered significant.
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Results |
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Increasing pressure constricted all segments of ILAs. As shown in Figure 2
, the elevation of renal
arterial pressure (RAP) from 80 to 120 mm Hg
decreased the diameter of distal ILAs by 2.2±0.6 µm (n=5).
Distal ILAs were further constricted at RAP of 160 mm Hg
(-5.0±0.7 µm). Similarly, intermediate ILAs manifested
decrements in their diameters in response to increasing RAP from 80 to
120 mm Hg (-2.7±1.1 µm; n=5). At RAP of 160 mm Hg,
the diameter of intermediate ILAs was reduced by 5.1±0.8 µm. In
contrast, although the elevation of RAP from 80 to 120 mm Hg did
not contract proximal ILAs, further pressure increments to 160
mm Hg elicited significant myogenic contraction (-3.3±1.2 µm;
n=5). Figure 3 describes the magnitude of
myogenic responsiveness plotted against basal ILA diameters at 80
mm Hg. There was a linear relationship between 2
parameters (r=0.92). ILAs with smaller diameters
manifested a greater degree of myogenic constriction.
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) and in the presence of diltiazem (
)
are shown. *Significant difference from respective basal value at
80 mm Hg.
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=0.28±0.03%/µm; n=15;
P<0.01 vs zero).
Although administration of diltiazem (10 µmol/L) failed to alter
basal diameters in all segments of ILAs at 80 mm Hg, it inhibited
myogenic responses of ILAs (Figure 2
). In distal ILAs, diltiazem
completely abolished myogenic constriction. The elevation of RAP from
80 to 160 mm Hg did not alter distal ILA diameter (0.0±0.6
µm; P<0.01 versus control response). Diltiazem also
prevented myogenic constriction of intermediate ILAs. In the presence
of diltiazem, pressure stimuli of 160 mm Hg did not decrease
intermediate ILA diameters (-1.1±0.7 µm; P<0.01
versus control). In addition, diltiazem blocked myogenic contraction of
proximal ILAs. At RAP of 160 mm Hg, proximal ILA diameter was
maintained (-1.3±0.8 µm; P<0.05 versus control).
Subsequent increase in potassium concentration did not alter distal
(from 29.1±3.0 to 28.9±3.3 µm), intermediate (from 49.7±3.0
to 49.0±3.5 µm), or proximal ILA diameters (from 76.4±5.9 to
75.8±6.0 µm), suggesting sufficient inhibition of L-type
voltage-dependent calcium channels by this dose of diltiazem.
Figure 4 depicts the effects of
gadolinium and NCDC on ILA myogenic responses. Under control
conditions, myogenic responses were well preserved in all segments of
ILAs. Thus, increasing RAP from 80 to 160 mm Hg elicited 17±2%,
10±2%, and 5±1% decrements of diameters in distal (-4.8±0.8
µm; n=6), intermediate (-4.4±0.6 µm; n=6), and proximal ILAs
(-3.8±1.0 µm; n=6), respectively. Gadolinium abolished
myogenic constriction of distal ILAs. In the presence of gadolinium,
the elevation of RAP from 80 to 160 mm Hg did not alter distal
ILA diameter (-1.0±1.1 µm; P<0.01 versus control).
In contrast, myogenic constriction of intermediate ILAs was partially
attenuated by gadolinium. Pressure stimuli of 160 mm Hg
significantly constricted intermediate ILAs by 2.2±0.7 µm
(P<0.05 versus control). Finally, gadolinium failed to
alter myogenic responsiveness of proximal ILAs. Increasing RAP from 80
to 160 mm Hg decreased the diameter of proximal ILAs by
3.1±0.6 µm (P=NS versus control). Figure 5 shows the inhibition by gadolinium of
ILA myogenic responsiveness plotted against basal ILA diameters at
80 mm Hg. There was an inverse relationship between 2
parameters (r=0.86). Gadolinium manifested
greater inhibitory effects on myogenic constriction in ILAs
with smaller diameters.
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) blocked myogenic constriction in
distal ILAs. Subsequent addition of NCDC (
) inhibited myogenic
contraction in intermediate and proximal ILAs. Controls are also shown
(
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Subsequent administration of NCDC (200 µmol/L), a phospholipase
C inhibitor, abolished residual myogenic contraction in
proximal and intermediate ILAs (Figure 4). Combined treatment with
gadolinium and NCDC blocked myogenic constriction of intermediate ILAs.
In the presence of both gadolinium and NCDC, raising RAP from 80 to
160 mm Hg did not alter intermediate ILA diameters (0.2±0.6
µm; P<0.01 versus control). At 80 mm Hg, NCDC
increased basal diameter of proximal ILAs from 79.3±5.2 to
85.8±6.2 µm (P<0.05). Furthermore, myogenic
contraction of proximal ILAs was prevented by the addition of NCDC
(0.0±0.8 µm [at 160 mm Hg]; P<0.05 versus
control). Subsequent addition of high-potassium media reduced distal,
intermediate, and proximal ILAs by 34±5%, 20±3%, and 7±2%,
respectively (P<0.01). These data suggest that at the doses
used, gadolinium or NCDC does not interact nonspecifically with
voltage-dependent calcium channels.
Since several lines of evidence indicate that phospholipase C could be
activated through gadolinium-sensitive
mechanisms,20 direct influences of NCDC on ILA
myogenic responses were assessed. Similar to the previous groups, all
segments of ILAs responded to pressure stimuli under control conditions
(Figure 6). Administration of NCDC
altered basal diameter of neither distal (from 26.4±2.8 to
26.6±2.6 µm; n=6) nor intermediate ILAs (from 49.4±2.8 to
50.7±2.9 µm; n=6) at RAP of 80 mm Hg. Furthermore, NCDC
did not alter myogenic responsiveness of distal ILAs. In the presence
of NCDC, increasing RAP from 80 to 160 mm Hg constricted distal
ILAs (-3.9±1.2 µm; P=NS versus control). However,
the addition of NCDC attenuated myogenic constriction of intermediate
ILAs. When treated with NCDC, the elevation of RAP from 80 to 120
mm Hg did not elicit constriction in intermediate ILAs, and the
diameter of intermediate ILAs was decreased only by 3.4±1.0 µm
at RAP of 160 mm Hg (P<0.05 versus control
[-5.4±0.9 µm]). In proximal ILAs, NCDC abolished myogenic
contraction. Basal diameter of proximal ILAs at 80 mm Hg was
increased by NCDC (from 75.2±4.3 to 78.3±4.5 µm; n=6;
P<0.05). Furthermore, alterations in RAP from 80 to
160 mm Hg failed to alter proximal ILA diameters (-0.2±1.1
µm; P<0.05 versus control).
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Figure 7 describes the effects of
staurosporine and thapsigargin on ILA myogenic responses.
Under control conditions, all segments of ILAs responded to increasing
RAP. In distal ILAs, neither staurosporine nor thapsigargin
altered basal diameter (from 25.6±3.3 to 26.0±3.5 µm; n=6) and
myogenic responsiveness, suggesting that these blockers possess little
effect on mechanosensitive cation channels and myosin light chain
kinase. In intermediate ILAs, myogenic responsiveness was not altered
by the administration of staurosporine but was attenuated
with thapsigargin. In the presence of thapsigargin, the elevation
of pressure from 80 to 160 mm Hg elicited only 6±2% reductions
in intermediate ILA diameters (-2.9±1.0 µm; n=6;
P<0.05 versus control [-5.1±1.0 µm]). In
proximal ILAs, treatment with staurosporine increased their
diameters at RAP of 80 mm Hg (from 77.8±5.3 to 80.9±5.5
µm; n=6; P<0.05). However, in the presence of
staurosporine, increasing pressure contracted proximal ILAs
(-4.5±0.8 µm [at 160 mm Hg]; P=NS versus
control). Subsequent addition of thapsigargin virtually abolished
myogenic contraction of proximal ILAs. Under the blockade of both
protein kinase C and calcium mobilization, raising pressure from 80 to
160 mm Hg did not elicit proximal ILA contraction
(-1.5±1.1 µm; P<0.01 versus control).
High-potassium media decreased distal (from 25.7±3.3 to 15.2±3.1
µm; P<0.01), intermediate (from 50.6±3.3 to
38.5±3.5 µm; P<0.01), and proximal ILA diameters
(from 81.8±5.5 to 72.1±5.6 µm; P<0.01).
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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ILAs arise from arcuate arteries near the corticomedullary junction and terminate at afferent arterioles in the cortex.21 ILAs taper along their length, varying in diameter from >90 µm near the arcuate artery to <30 µm at the terminal segment. Thus, ILAs constitute important resistance vessels relating to renal autoregulation. Indeed, intraluminal pressure within proximal ILAs near the arcuate artery is directly related to systemic blood pressure,11 whereas that within distal ILAs at the terminal segment is partially autoregulated.10 In accordance, recent investigations using various approaches demonstrated that increasing RAP elicited ILA constriction.5 8 18 22 However, the mechanisms mediating autoregulatory responses of ILAs were not fully characterized. Furthermore, differing mechanisms may underlie myogenic responses in distinct segments of ILAs.
ILAs appear to possess segmental differences in the magnitude of
increase in vascular resistance responding to elevating pressure. Since
vascular resistance is related to 1/radius4
(Hagen-Poiseuille equation), vessels with smaller diameters should
provide greater vascular resistance. Furthermore, our results are
consistent with observations that vessels with smaller calibers
manifest stronger myogenic responses1 and
indicate that ILAs with smaller diameters manifested greater degree of
myogenic constriction (Figure 3). Thus, the present data support
the previous findings that intravascular pressure in distal ILAs was
partially autoregulated10 and further suggest
that myogenic constriction of ILAs, especially distal segments,
substantively participates in total renal vascular resistance
adjustments responding to pressure.
In the present study we demonstrated that myogenic constriction in all segments of ILAs was prevented by diltiazem. The present results support previous observations by Casellas and Bouriquet22 that nimodipine inhibited myogenic constriction of ILAs and arcuate arteries. Furthermore, we showed that thapsigargin did not alter myogenic constriction of distal ILAs. The observations that high-potassium media constricted ILAs in the presence of thapsigargin suggest that calcium entry through L-type calcium channels increases cytosolic calcium sufficient to induce ILA constriction. Our findings, however, differ from those of Inscho et al23 that thapsigargin inhibited pressure-induced afferent arteriolar constriction. Because the afferent arteriole is the target of TGF9 and because calcium mobilization plays an important role in transducing TGF,4 23 the variance in observed sites may account for the discrepancy. Calcium antagonists nullify TGF signals at the effector level.4 Finally, recent results demonstrated that the autoregulation of total renal blood flow was virtually abolished by the blockade of voltage-dependent calcium channels.4 24 Collectively, these results indicate that as afferent arterioles,3 9 the activation of voltage-dependent calcium channels mediates ILA myogenic constriction, and they suggest that L-type calcium channels play a crucial role in autoregulatory adjustments of renal vascular resistance.
Although there seems to be consensus on a mediatory role of voltage-dependent calcium channels in renal autoregulation,4 the ionic mechanisms mediating activation of L-type calcium channels by pressure are poorly understood. We have previously provided evidence that pressure-induced activation of mechanosensitive cation channels, a membrane-delimited process, underlies afferent arteriolar myogenic constriction.3 Although gadolinium may interact with L-type calcium channels, which are essential for myogenic constriction in distal ILAs, high-potassium media constricted distal ILAs in the presence of gadolinium. Furthermore, our data indicated that proximal ILA myogenic contraction was inhibited by diltiazem but not gadolinium. In addition, while calcium entry through gadolinium-sensitive channels may stimulate phospholipase C,20 our demonstrations that NCDC itself did not significantly alter distal ILA myogenic constriction mitigate against a dominant role of phospholipase C in distal ILA myogenic constriction. Thus, these findings suggest that in a manner similar to that of afferent arterioles,3 pressure stimuli increase the open probability of mechanosensitive cation channels on distal ILAs, thereby eliciting membrane depolarization and activation of voltage-dependent calcium channels.
In contrast to distal ILAs, gadolinium exhibited little inhibitory effect on myogenic contraction of proximal ILAs, suggesting a small role of membrane-delimited mechanism in this response. Roman and Harder12 have demonstrated that increasing pressure raises both inositol trisphosphate and diacylglycerol in renal arteries. They suggest that in a manner similar to that of aortic myocytes,2 pressure stimuli activate phospholipase C in renal arteries, thereby mediating myogenic contraction. In agreement, we showed that NCDC, a phospholipase C inhibitor, abolished myogenic contraction of proximal ILAs. Although the addition of either NCDC or staurosporine increased proximal ILA diameters at RAP of 80 mm Hg, myogenic contraction was blocked only by NCDC, validating that ILA dilation itself does not impair myogenic contraction. The present data provide evidence that phospholipase C mediates myogenic contraction of proximal ILAs and suggest that at the RAP of 80 mm Hg, pressure-induced activation of phospholipase C is already operative in proximal ILAs.
Since phospholipase C produces 2 important second messengers, we assessed the effects of staurosporine, a protein kinase C blocker,19 and thapsigargin, which depletes calcium store,16 on myogenic responses. Osol et al25 suggest the participation of protein kinase C in the development of basal tone. Similarly, we have shown that the administration of staurosporine elicited vasodilation of proximal ILAs at RAP of 80 mm Hg. Ample evidence indicates that protein kinase C enhances sensitivity of contractile elements to a given concentration of cytosolic calcium. Indeed, our previous data suggest that endothelin-induced activation of protein kinase C increases the sensitivity of contractile elements to calcium in preglomerular microvasculature.19 Collectively, these data suggest that protein kinase C constitutes a determinant of basal tone in proximal ILAs. On the other hand, Roman and Harder12 suggested that pressure induces intracellular calcium mobilization in vascular smooth muscle. The present observations that the treatment with thapsigargin blocked myogenic contraction of proximal ILAs are compatible with previous findings2 12 and suggest a pivotal role of calcium mobilization in activating voltage-dependent calcium channels on this ILA segment by pressure. Elevation of cytosolic calcium could elicit membrane depolarization directly by opening chloride channels on proximal ILAs and/or indirectly by closing potassium channels through the stimulation of phospholipase A2.12 14 26
Intermediate ILAs appear to exhibit characteristics between those of
distal and proximal ILAs. In the present study we have
demonstrated that either gadolinium or NCDC attenuated but did not
block myogenic constriction of intermediate ILAs. However,
simultaneous treatment with both gadolinium and NCDC
abolished intermediate ILA myogenic constriction. Our data provide
evidence that both membrane-delimited and phospholipase C–dependent
processes are required for full activation of voltage-dependent calcium
channels in intermediate ILAs during myogenic stimulation. Since
gadolinium exhibited greater inhibitory effects on myogenic
constriction in ILAs with smaller diameter (Figure 5),
gadolinium-sensitive mechanosensitive cation channels may prevail in
small ILAs. Taken together, these findings suggest that intermediate
ILAs constitute transitional sites regarding the mechanisms underlying
myogenic responses.
A caveat should be considered. Although calcium entry through mechanosensitive cation channels may trigger phospholipase C,20 our data demonstrated that gadolinium failed to induce substantial alterations in myogenic contraction of proximal ILAs. Kulik et al27 suggested that physical stimuli stimulate phospholipase C through the pathways insensitive to pertussis toxin. As reviewed recently,1 Gq proteins may be involved in triggering phospholipase C during myogenic activation. Clearly, further studies are required to elucidate precise mechanisms of the activation of phospholipase C by pressure stimuli.
In summary, the present data indicate that mechanisms mediating myogenic responses differ among distinct segments of ILAs. In addition, our results suggest that increasing pressure gates mechanosensitive cation channels, thereby eliciting membrane depolarization and activation of voltage-dependent calcium channels in distal ILAs. Finally, our findings provide evidence that pressure-induced stimulation of phospholipase C mediates myogenic contraction of proximal ILAs.
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Acknowledgments |
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This study was supported in part by a grant from the Ministry of Education and Culture, Japan.
Received May 25, 1998; first decision June 15, 1998; accepted August 17, 1998.
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A. C. Schroeder, J. D. Imig, E. A. LeBlanc, B. T. Pham, D. M. Pollock, and E. W. Inscho Endothelin-Mediated Calcium Signaling in Preglomerular Smooth Muscle Cells Hypertension, January 1, 2000; 35(1): 280 - 286. [Abstract] [Full Text] [PDF]
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