(Hypertension. 1996;28:604-608.)
© 1996 American Heart Association, Inc.
Articles |
Increased Wall-Lumen Ratio of Mesenteric Vessels From the Spontaneously Hypertensive Rat Is Not Associated With Increased Contractility Under Isobaric Conditions
the Department of Medicine, Manchester (UK) Royal Infirmary.
Correspondence to Dr Ashley S. Izzard, PhD, Department of Medicine, Manchester Royal Infirmary, Oxford Rd, Manchester, UK, M13 9WL.
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Abstract |
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We investigated the morphological (wall-lumen ratio) and contractile characteristics of distal mesenteric arteries from spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) controls at a distending pressure of 63% of the mean aortic pressure of each rat using a pressure arteriograph. The wall-lumen ratios obtained were compared with those obtained at a pressure of 100 mm Hg. Experiments were carried out at 5 and 20 weeks. Mean aortic pressure of SHR was significantly increased at 5 weeks compared with that of WKY and was further increased by 20 weeks. At 63% of mean aortic pressure, no difference in the wall-lumen ratio of the arteries was observed between strains at 5 weeks; at 20 weeks, the wall-lumen ratio of SHR arteries was significantly increased compared that in WKY arteries. The wall-lumen ratio of SHR vessels did not differ at 63% mean aortic pressure compared with 100 mm Hg at either 5 or 20 weeks, whereas this parameter was significantly reduced in WKY vessels at 100 mm Hg compared with 63% mean aortic pressure at 5 and 20 weeks. In the presence of spontaneous myogenic tone, there was a borderline reduction in the lumen diameter of SHR vessels compared with WKY vessels and with increasing norepinephrine concentrations at 5 weeks. At 20 weeks, lumen diameter between strains did not differ in the presence of myogenic tone nor with increasing norepinephrine concentrations. Similar results were obtained when vessels from both rat strains were pressurized to 80 mm Hg. Thus, the increased wall-lumen ratio in the distal mesenteric arteries from adult SHR compared with those from WKY is not associated with an increased contractility under isobaric conditions when studied at physiological distending pressure.
Key Words: rats, inbred SHR • mesenteric arteries • pressure
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Introduction |
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The majority of in vitro investigations of the morphological and contractile properties of small arteries in hypertension have been performed with either an isometric wire myograph or an isobaric pressure-perfusion system.1 In the former case, arteries are set to a resting internal circumference at which near-maximal active tension development occurs when fully activated, and morphological parameters have been defined at that setting.2 Similarly, under isobaric conditions, vessels have been studied at an optimal intraluminal pressure, ie, one at which the greatest change in lumen diameter is observed when arteries are stimulated.3 4 Although direct comparisons of the two techniques have revealed significant differences in small-artery morphology5 and function,6 7 the pressure system is undoubtedly a more appropriate technique for investigation of the pathophysiology of small arteries. Nevertheless, in hypertension research, in vivo distending pressures would be a more physiological setting for the study of small-artery structure and function rather than setting arteries to conditions for maximal responsiveness. In addition, morphological parameters are highly dependent on the distending pressure, in particular, the wall-lumen ratio,5 which is considered to be the most important structural determinant of vascular contractility, in that a larger wall-lumen ratio results in a more pronounced luminal narrowing for a given degree of smooth muscle shortening.8
Recently, Christensen and Mulvany9 have measured blood pressure at the base of the mesenteric arcade of conscious adult spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) controls. For each rat strain, the pressure when expressed as a percentage of mean aortic pressure (MAP) was the same (63%); thus, the distal mesenteric pressure is increased in SHR in proportion to the increased MAP. Using this information, we decided to determine distal mesenteric artery wall-lumen ratio and contractility to norepinephrine of SHR vessels at 5 weeks when hypertension is developing and 20 weeks when hypertension is established compared with WKY controls.
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Methods |
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Male SHR and WKY (4 weeks old) were obtained from Charles River, Kent, UK. Abdominal aortic blood pressure was determined as described in detail previously.10 Briefly, during anesthesia, polyethylene catheters were inserted into the left femoral artery of the rats, and the tip was advanced into the abdominal aorta. Twenty-four hours later, blood pressure recordings were made in unrestrained, conscious rats under quiet, resting conditions. MAP was calculated as diastolic pressure plus one-third pulse pressure.
Isolation of Arteries
On the day of the study, rats were killed by stunning followed by cervical dislocation. The intestine was exposed by an abdominal incision, and a segment of the proximal jejunum with attached mesentery was excised and placed in ice-cold physiological salt solution (PSS) with the following composition (mmol/L): NaCl 119, KCl 4.7, NaHCO3 25, KH2PO4 1.17, MgSO4 1.17, EDTA 0.026, CaCl2 1.6, and glucose 5.5.
Distal mesenteric arteries (sixth-generation branches), approximately 1 to 2 mm long, were freed from adherent adipose tissue, removed, and placed in a pressure arteriograph bath chamber (Living Systems Instrumentation).11 The artery was pressurized to 63% of the rat's MAP and checked for leaks. A stable pressure recording while the pressure-servo system was turned on to manual confirmed the absence of leaks. Any artery that leaked was discarded. The artery was visualized on a TV monitor, and inner diameter and wall thickness were determined with a Video Dimension Analyzer (Living Systems) as previously described.11 At maximal activation with norepinephrine, the lumen diameter was measured with a calibrated ruler placed against the TV screen, as there is insufficient difference in the optical density of the walls and lumen for measurement of inner diameter with the dimension analyzer. Because vasomotion was typically associated with maximal stimulation with norepinephrine, mean diameter was calculated from the minimum and maximum diameter recorded over 2 minutes during the plateau phase of contraction. The magnitude of the vasomotion was 9±3.4 µm (range, 19 to 28) and 9±1.8 µm (range, 25 to 34) for vessels from adult SHR and WKY, respectively, at 63% MAP and exposed to 10 µmol/L norepinephrine. Pressure and inner diameter were recorded on a chart recorder. The temperature of the arteriograph bath chamber was increased to 37°C with a circulating water heater. The arterial segment was left to equilibrate for 1 hour; during this time, vessels developed spontaneous tone. The arteriograph bath chamber was superfused with PSS from a reservoir gassed with 5% CO2/95% O2, pH 7.4 to 7.45, at a superfusion rate of 20 mL/min. Superfusion rate has no effect on basal tone within the range tested of 5 to 40 mL/min.
Concentration-response curves to 0.001 to 10 µmol/L norepinephrine (Sigma Chemical Co) were obtained by cumulative addition of norepinephrine to the superfusate. Arteries were stimulated for at least 4 minutes at each concentration so that the responses had time to plateau. Afterward, the vessels were superfused with Ca2+-free PSS containing 1 mmol/L EGTA for 30 minutes to obtain the passive diameter. After wall thickness and lumen diameter had been noted, the pressure was set to 100 mm Hg so that morphological characteristics of the two strains could be compared at in vivo distending pressures and at an equivalent pressure. From the wall thickness and lumen diameter recorded, the wall-lumen ratio was calculated and expressed as a percentage.
Another series of experiments was carried out as above, but intraluminal pressure was set to 80 mm Hg for all vessels from both rat strains and the norepinephrine concentration ranged from 0.01 to 10 µmol/L. Only 20-week-old rats were chosen for this investigation.
Data and Statistics
Contractile responses to norepinephrine are expressed as the mean diameter in microns. Statistical comparisons between and within strains were performed with Student's unpaired and paired t tests, respectively. Data are presented as mean±SE.
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Results |
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At 5 weeks of age, SHR had significantly elevated MAP compared with WKY controls (119±3 versus 98±3 mm Hg, P<.001, n=8). Pressures at the base of the mesenteric arcade were 75±2 and 62±2 mm Hg in SHR and WKY, respectively. In the established stage of hypertension at 20 weeks, MAP of SHR was 161±5 mm Hg compared with 116±3 mm Hg in WKY (P<.01, n=6 and 8, respectively), and calculated distal mesenteric pressures were 103±2 and 72±2 mm Hg in SHR and WKY, respectively.
At 5 weeks, wall-lumen ratio between the strains did not differ in the passive condition when set to 63% MAP. When compared at the same distending pressure (100 mm Hg), the wall-lumen ratio of SHR vessels was 20% greater than that of WKY vessels, although it was not significantly different (P=.08). The wall-lumen ratio of SHR arteries was not different at a distending pressure of 63% MAP (75 mm Hg) compared with at 100 mm Hg. On the other hand, the wall-lumen ratio of WKY vessels was significantly (P<.05, Table 1
) reduced at 100 mm Hg compared with that at 63% MAP (62 mm Hg).
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At 20 weeks, the wall-lumen ratio was significantly different in the passive condition between strains compared with that at 63% MAP (103 and 73 mm Hg, SHR and WKY, respectively) and at 100 mm Hg distending pressure (P<.05, Table 1
). Table 1 shows that within strains, the wall-lumen ratio of SHR vessels did not differ at 63% MAP (105 mm Hg) compared with at 100 mm Hg, whereas the wall-lumen ratio of WKY vessels was significantly reduced at 100 mm Hg compared with at 63% MAP (73 mm Hg).
Fig 1 shows the diameter of vessels in the passive condition with spontaneous myogenic tone present and increasing norepinephrine concentrations at 5 weeks at 63% MAP. At maximal dilation, the lumen diameter of SHR vessels was significantly reduced compared with that of WKY vessels. In the presence of spontaneous tone, the difference in lumen diameters was of borderline statistical significance between strains (P=.08), and the change in diameter in response to norepinephrine was not different between strains. At 20 weeks, the lumen diameter of SHR vessels tended to be smaller under passive conditions compared with that of WKY vessels but was not significantly different (P=.07). In the presence of spontaneous myogenic tone, lumen diameters were not different, nor were the reductions in lumen diameter with increasing norepinephrine concentrations (Fig 2).
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We considered the possibility that the increased wall-lumen ratio did not increase the contractility of small arteries from SHR at 20 weeks in terms of lumen diameter reduction because of the greater distending pressure. Furthermore, although morphological comparisons are usually made when vessels are devoid of active tone, it is possible that the increased wall-lumen ratio of SHR vessels at maximal dilation may not be observed in the presence of spontaneous tone. Thus, we repeated the experiments at 80 mm Hg pressure, which is less than 63% MAP for SHR vessels but greater than 63% MAP for WKY vessels. This setting also does not deviate much from physiological distending pressures for either rat strain, in contrast to previous studies of upstream mesenteric arteries. In the presence of spontaneous tone at 80 mm Hg, the wall-lumen ratio was significantly increased in SHR compared with WKY as well as in the absence of tone (Table 2). In the absence of spontaneous tone, the lumen diameters of SHR arteries were significantly reduced compared control vessels. Lumen diameters were not significantly different between strains in the presence of spontaneous tone or with increasing norepinephrine concentrations (Fig 3).
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Discussion |
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This study demonstrates that the contractility of distal mesenteric arteries to norepinephrine is not increased during the developing and established stages of hypertension in SHR compared with WKY controls under isobaric conditions at physiological pressures in vitro. This finding is at variance with the observation of a greater contractility of the mesenteric vasculature from mature SHR in terms of active tension or "effective pressure" than that seen in vessels from normotensive controls, a finding noted with the use of wire-mounted preparations.1 2 The lack of any difference in Ca2+ handling in the mesenteric artery wall between strains when stimulated with norepinephrine12 13 lends further support to observations regarding the importance of structural changes of hypertensive mesenteric arteries for the increased contractility observed under isometric conditions.1 2 13 Although the above indexes of contractility are not comparable with changes in lumen diameter, the latter is probably more important in relation to the control of cardiovascular function than the ability of blood vessels to generate active tension under isometric conditions.14 It might be argued that the lack of differences in responsiveness to norepinephrine in mesenteric arteries from SHR compared with vessels from normotensive control rats at 20 weeks does reflect their greater contractility because the MAP and distal mesenteric distending pressure (63% MAP) are increased. However, the lack of difference in the response to norepinephrine between strains when both sets of vessels are pressurized to 80 mm Hg makes this explanation unlikely. Furthermore, differences in wall-lumen ratio observed in 20-week-old SHR compared with WKY in the absence of tone were also observed in the presence of spontaneous myogenic tone (Table 2
); thus, a lack of wall-lumen ratio increase in the presence of spontaneous tone does not explain the lack of increased contractility of the vessels from the hypertensive rats. Under isobaric conditions, constriction reduces wall tension according to the law of Laplace. A reduction in wall tension or smooth muscle shortening reduces force generation, thereby having a negative feedback action on lumen diameter reduction,15 16 17 which clearly cannot occur under isometric conditions. Thus, equivalent concentrations of norepinephrine may not necessarily result in an equal degree of smooth muscle shortening in vessels from SHR and WKY, masking the inherent differences in contractility between the strains that results from the differing wall-lumen ratios.
We chose norepinephrine as an agonist because it is a physiologically relevant vasoconstrictor agent. However, norepinephrine is a mixed adrenoceptor agonist, and differences in constrictor and dilator components between the strains (ie, 
-adrenoreceptor–mediated constriction and ß-adrenoreceptor–mediated dilation) could influence the results. Indeed, the ß-adrenoreceptor–mediated relaxant component of the norepinephrine response has been shown to be impaired in SHR. Although this is more prominent in femoral than mesenteric strips,18 19 such an abnormality in the resistance vasculature of the SHR would be expected to enhance the constrictor response to norepinephrine. Therefore, it is unlikely that a structurally determined exaggerated lumen reduction of SHR mesenteric vessels compared with WKY vessels when stimulated with norepinephrine was obscured as a consequence of the use of a mixed adrenoceptor agonist as opposed to, for example, a pure 1-adrenoreceptor agonist as the constrictor agent. A further consideration is that the circulating PSS was gassed with 5% CO2/95% O2, and such unphysiological oxygen levels could conceivably alter the results. Nevertheless, we think it unlikely that the gas mixture used would have a differential effect on the contractility of vessels from the two strains, especially when greater contractile responses to norepinephrine on a wire myograph for SHR mesenteric arteries compared with control arteries are observed under identical gassing conditions.2
The wall-lumen ratio was not significantly increased in SHR mesenteric arteries at 5 weeks compared with WKY arteries when the distending pressure was either 63% MAP or 100 mm Hg. In contrast, at 20 weeks, the wall-lumen ratio of the hypertensive vessels was significantly increased compared with that in controls at both 63% MAP and 100 mm Hg. Nevertheless, it would be misleading to conclude that the distending pressure does not influence the results. At both 5 and 20 weeks, the wall-lumen ratio of the WKY mesenteric arteries was significantly reduced at 100 mm Hg compared with at 63% MAP (Table 1). Also at 5 weeks, there was a 2% (not significant) increase in the wall-lumen ratio of SHR vessels compared with WKY vessels at 63% MAP pressure. At 100 mm Hg pressure, the difference was 23% and of borderline significance. In a previous study,10 the difference in wall-lumen ratio at 100 mm Hg distending pressure between strains was highly significant at 5 weeks; failure to attain statistical significance at the 5% level in the present study probably reflects a type 2 error. Pressure of 100 mm Hg was chosen for measurement of the wall-lumen ratio of the vessels at equal distending pressure because other investigators have used it for standard comparisons.1 If the equivalent distending pressure chosen had been lower, eg, 30 to 40 mm Hg, as used by our group4 and other investigators,3 the differences in wall-lumen ratio compared with 63% MAP may have been greater because (1) the relationship between passive lumen diameter and pressure is quite steep at lower pressures and (2) there is much less longitudinal distension at lower compared with higher pressures.
The distal mesenteric vessel intraluminal pressure of 63% of the rat's MAP was chosen on the basis of the measurement of intravascular pressure at the base of mesenteric arcades in conscious, unrestrained rats and is in good agreement with servo-null pressure measurements from the exteriorized intestine of anesthetized rats.20 21 Such data obtained from adult rats may not apply to rats at 5 weeks of age; however, in the absence of any quantitative data at this age, we chose 63% of the MAP of each rat as for the adult rats.
Experiments with constant flow–perfused vascular beds demonstrate a greater pressor response to norepinephrine in SHR compared with controls, and this has been interpreted as evidence for an increased wall-lumen ratio of the resistance vessels.8 22 In the skeletal muscle vasculature in hypertension, in situ measurements indicate that such structural changes are located in the proximal resistance vasculature23 and therefore cannot solely account for the increased resistance of the whole bed, whereas in the distal microvasculature, there is evidence of an elevation in vascular tone and rarefaction.23 24 25 Addressing this issue, Prewitt et al26 performed pressure-flow curves of the hindquarter bed of the SHR compared with controls while measuring the diameter of cremaster arterioles. Vessels were also fixed at physiological distending pressures for morphological analysis. These investigators observed an increased wall-lumen ratio caused by medial hypertrophy of the cremaster arterioles from the SHR compared with WKY and suggested that this structural alteration accounts for the elevated maximal response of the SHR hindquarters to norepinephrine compared with normotensive rats; however, they did not observe a greater change in lumen diameter of SHR compared with WKY vessels for a given increase in the norepinephrine concentration. This similarity with the findings in distal mesenteric arteries in the present study may be coincidental because iontophoretic application of norepinephrine to SHR cremaster arterioles in situ reveals a hyperresponsiveness compared with WKY arterioles,24 and no such difference between strains has been observed for proximal intestinal arterioles.27 Furthermore, with regard to constant flow–perfused vascular beds at the flow rates used by other investigators, eg, 10 mL/min per 100 g for rat hindquarters,22 26 the perfusion pressure is very low in the absence of norepinephrine or any other vasoconstrictor, and so the resistance vessels would not possess significant myogenic tone, unlike the in vivo situation. The absence of a pressure rise after washout of papaverine in the perfused hindlimb preparation22 supports this suggestion. Also, as the norepinephrine concentration is increased, the perfusion pressures attained far exceed the MAP for both normotensive and hypertensive rats and as such represent a nonphysiological situation.
Whole-animal studies in both SHR28 29 and renovascular hypertension30 have failed to demonstrate amplified pressor responses to 1-adrenoreceptor agonists and angiotensin II compared with controls. It has been suggested that the amplifier consequences of an increased wall-lumen ratio are offset by other regulatory mechanisms in vivo.29 Given our findings under isobaric conditions in vitro, we suggest that the increased wall-lumen ratio at least of the distal mesenteric vasculature from the adult SHR is not associated with an increased contractility in terms of lumen diameter change. Furthermore, in the established but not developing stage of hypertension, the structurally reduced lumen diameter of the SHR mesenteric arteries, ie, the lumen diameter in the absence of tone, is no longer apparent in the presence of spontaneous myogenic tone and with increasing norepinephrine concentrations. This suggests that structural changes in small mesenteric arteries from the SHR may be of minor significance in the maintenance of hypertension.
In conclusion, we found no evidence for an increased contractility to norepinephrine in isolated pressurized distal mesenteric arteries from the SHR set to physiological pressures when changes in lumen diameter are recorded in vitro compared with WKY control vessels at 5 or 20 weeks of age, despite a significantly increased wall-lumen ratio of the SHR mesenteric vessels at 20 weeks. Therefore, the pathophysiological consequences of an increased wall-lumen ratio in hypertensive disease must be interpreted with caution.
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Acknowledgments |
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This work was supported by the British Heart Foundation and the Medical Research Council.
Received December 26, 1995; first decision January 29, 1996; accepted May 16, 1996.
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References |
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1. Mulvany MJ, Aalkjaer C. Structure and function of small arteries. Physiol Rev. 1990;70:921-961.
2.
Mulvany MJ, Hansen PK, Aalkjaer C. Direct evidence that the greater contractility of resistance vessels in spontaneously hypertensive rats is associated with a narrowed lumen, a thickened media, and an increased number of smooth muscle cell layers. Circ Res. 1978;43:854-864.
3.
Dohi Y, Luscher TF. Endothelin in hypertensive resistance arteries: intraluminal and extraluminal dysfunction. Hypertension. 1991;18:543-549.
4.
Falloon BJ, Bund SJ, Tulip JR, Heagerty AM. In vitro perfusion studies of resistance artery function in genetic hypertension. Hypertension. 1993;22:486-495.
5. Lew JM, Angus JA. Wall thickness to lumen diameter ratios of arteries from SHR and WKY: comparison of pressurized and wire-mounted preparations. J Vasc Res. 1992;29:435-442.[Medline] [Order article via Infotrieve]
6.
Dunn WR, Wellman GC, Bevan JA. Enhanced resistance artery sensitivity to agonists under isobaric compared with isometric conditions. Am J Physiol. 1994;266:H147-H155.
7.
Falloon BJ, Stephens N, Tulip JR, Heagerty AM. Comparison of small artery sensitivity and morphology in pressurized and wire-mounted preparations. Am J Physiol. 1995;268:H670-H678.
8.
Folkow B. Physiological aspects of primary hypertension. Physiol Rev. 1982;62:347-503.
9.
Christensen KL, Mulvany MJ. Perindopril changes the mesenteric pressure profile of conscious hypertensive and normotensive rats. Hypertension. 1994;23:325-328.
10.
Izzard AS, Bund SJ, Heagerty AM. Myogenic tone in mesenteric arteries from spontaneously hypertensive rats. Am J Physiol. 1996;270:H1-H6.
11. Halpern W, Osol G, Coy GS. Mechanical behaviour of pressurized in vitro prearteriolar vessels determined with a video system. Ann Biomed Eng. 1984;12:463-479.[Medline] [Order article via Infotrieve]
12. Bukoski RD, Lastelic BA, Xue H, Li J, Bian K. Intracellular Ca2+ and force generation determined in resistance arteries from normotensive and hypertensive rats. J Hypertens. 1994;12:15-21.[Medline] [Order article via Infotrieve]
13.
Bian K, Bukoski RD. Myofilament calcium sensitivity of normotensive and hypertensive resistance arteries. Hypertension. 1995;25:110-116.
14. Cox RH. Mechanics of blood vessels: conduit arteries. In: Stephens NL, ed. Smooth Muscle Contraction. New York, NY: Marcel Dekker; 1984:405-425.
15. Speden RN, Warren DM. The interaction between noradrenaline activation and distension activation of the rabbit ear artery. J Physiol. 1986;325:283-302.
16.
Jackson PA, Duling BR. Myogenic response and wall mechanics of arterioles. Am J Physiol. 1989;257:H1147-H1155.
17. VanBavel E, Mulvany MJ. Role of wall tension in the vasoconstrictor response of cannulated rat mesenteric arteries. J Physiol. 1994;447:408-418.
18.
Asano M, Aoki K, Matsuda T. Reduced beta adrenoceptor interactions of norepinephrine enhance contraction in the femoral artery from spontaneously hypertensive rats. J Pharmacol Exp Ther. 1982;223:207-214.
19. Asano M, Masuzawa K, Matsuda T, Asano T. Decreased responsiveness of ß-adrenoceptor agonists in arterial strips from spontaneously hypertensive rats is not associated with alterations in ß-adrenoceptors. J Hypertens. 1991;9:607-613.[Medline] [Order article via Infotrieve]
20.
Bohlen HG. Intestinal microvascular adaptation during maturation of spontaneously hypertensive rats. Hypertension. 1983;5:739-745.
21.
Meininger GA, Fehr KL, Yates MB, Borders JL, Granger HG. Hemodynamic characteristics of the intestinal microcirculation in renal hypertension. Hypertension. 1986;8:66-75.
22. Folkow B, Hallback M, Lundgren Y, Weiss L. Background of increased flow resistance and vascular reactivity in spontaneously hypertensive rats. Acta Physiol Scand. 1970;80:93-106.[Medline] [Order article via Infotrieve]
23.
Ono Z, Prewitt RL, Stacey DL. Arteriolar changes in developing and chronic stages of two-kidney, one clip hypertension. Hypertension. 1989;14:36-43.
24. Bohlen HG. Arteriolar closure mediated by hyperresponsiveness to norepinephrine in hypertensive rats. Am J Physiol. 1979;5:H157-H164.
25. Hutchins PM, Darnell AE. Observations of a decreased number of small arterioles in spontaneously hypertensive rats. Circ Res. 1974;34(suppl I):I-161-I-165.
26.
Prewitt RL, Reilly CK, Wang DH. Pressure-flow curves reflect arteriolar responses in perfused rat hindquarters. Hypertension. 1994;23:223-228.
27.
Bohlen HG, Lash JM. Active and passive regulation in spontaneously hypertensive rats. Hypertension. 1994;23:757-764.
28.
Touw KB, Haywood JR, Shaffer RA, Brody MJ. Contribution of the sympathetic nervous system to vascular resistance in conscious young and adult spontaneously hypertensive rats. Hypertension. 1980;2:408-418.
29. Leenen FHH, Yuan B, Tsoporis J, Lee RMKW. Arterial hypertrophy and pressor responsiveness during development of hypertension in spontaneously hypertensive rats. J Hypertens. 1994;12:23-32.[Medline] [Order article via Infotrieve]
30.
Marks ES, Bing RF, Thurston H, Russell GI, Swales JD. Responsiveness to pressor agents in experimental renovascular and steroid hypertension. Hypertension. 1982;4:238-244.
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