Alterations in renal vascular resistance and reactivity in spontaneous hypertension of rats

Berecek, Kathleen H.; Schwertschlag, Ullrich; Gross, F.

doi:10.1152/ajpheart.1980.238.3.h287

Cited by 54 publications

(51 citation statements)

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“…Further, the aggravated renal vasoconstriction is suggested to be a key pathomechanism for the development of hypertension in SHR (31,32) and SHRSP (33). Consistent with these reports, the RVR was greater in SHRSP and SHRSPwch1.0, both of which were phenotypically hypertensive, than in WKYpch1.0 and WKY.…”

Section: Discussionsupporting

confidence: 74%

Sympathetic Regulation of the Renal Functions in Rats Reciprocally Congenic for Chromosome 1 Blood Pressure Quantitative Trait Locus

et al. 2008

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Section: Discussionsupporting

confidence: 74%

Sympathetic Regulation of the Renal Functions in Rats Reciprocally Congenic for Chromosome 1 Blood Pressure Quantitative Trait Locus

et al. 2008

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“…Our observations are consistent with previous reports indicating that renal vascular resistance and the vascular reactivity to vasoconstrictors are elevated in SHR. 4 -5 However, they do not contradict the results of other studies indicating that the wall-to-lumen ratio of the renal vasculature is elevated in SHR. 8 Hypertrophy of the muscle layers in renal vessels, indeed, could contribute to the elevated renal vascular tone in SHR and still be consistent with present results in low calcium solutions as long as the thickening of the vascular wall does not narrow the lumen of maximally dilated vessels.…”

Section: Discussionmentioning

confidence: 50%

Enhanced vascular tone in the renal vasculature of spontaneously hypertensive rats.

et al. 1990

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The renal microvascular responses of Wistar-Kyoto and spontaneously hypertensive rats to changes in perfusion pressure were compared using a juxtamedullary nephron microvascular preparation perfused in vitro with a physiological salt solution containing 5% albumin. In the spontaneously hypertensive rats, the internal diameters of arcuate and interlobular arteries and the proximal and distal afferent arterioles averaged 307±26, 52±2, 24±0.9, and 22±1.2 ftm, respectively, at 80 mm Hg. They were 18-35% smaller (p<0.05) than the corresponding vessels measured in Wistar-Kyoto rats. In low calcium media, the arcuate and interlobular arteries and the proximal and distal afferent arterioles of spontaneously hypertensive rats exhibited a greater dilation than the vessels of Wistar-Kyoto rats. These observations suggest that the diameters of the preglomerular vasculature of the spontaneously hypertensive rats are reduced because of an elevated vascular tone rather than structural changes narrowing the lumen of these vessels. These results suggest that enhanced vascular tone in the preglomerular vasculature of juxtamedullary nephrons may contribute to the elevated renal medullary vascular resistance and resetting of the pressure-natriuretic relation previously observed in spontaneously hypertensive rats. (Hypertension 1990;16:648-654) R enal transplantation studies have indicated that some form of renal dysfunction underlies the development of genetic hypertension.12 Nevertheless, the factors that contribute to the "resetting of the kidney in hypertension" remain unknown. Numerous differences in renal function of spontaneously hypertensive rats (SHR) and WistarKyoto (WKY) rats have been described; these include an elevated renal vascular resistance, 3 -5 enhanced renal vascular reactivity to vasoconstrictors, 4 -5 enhanced tubuloglomerular feedback response, 6 and structural changes that increase the wall-to-lumen ratio in the renal vasculature.78 Because most of these changes have been identified in the established phase of hypertension, it remains unclear whether these changes are a cause or a consequence of the disease.We recently reported that the pressure-natriuretic response is blunted in SHR and Dahl salt-sensitive rats before the development of hypertension. 910 In the SHR, the abnormality in the pressure-natriuretic response is associated with a reduction in papillary blood flow 11 and renal interstitial hydrostatic pressure. 12 These observations suggest that an elevation in renal medullary vascular resistance may participate in the resetting of the renal function toward higher pressures in SHR. 11The factors responsible for reducing papillary blood flow in SHR are unknown. Medullary blood flow is derived exclusively from the perfusion of deep nephrons. Thus, structural changes that narrow the lumen of the preglomerular vasculature of juxtamedullary nephrons or alterations in the reactivity of these vessels could be responsible for the!, reduction of papillary blood flow in SHR. The recent development of the in ...

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“…39 -41 A similar determinacy is likely in the SHRSP, in which the renal vasoconstrictive response to angiotensin II is also exaggerated. 42 Thus, in the SHRSP, the Cl Ϫ component of dietary NaCl might dominantly determine the expression of salt sensitivity by determining the extent to which the renal afferent arteriole is further narrowed.…”

Section: Discussionmentioning

confidence: 99%

Chloride-Dominant Salt Sensitivity in the Stroke-Prone Spontaneously Hypertensive Rat

et al. 2005

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Abstract-We tested the hypothesis that in the stroke-prone spontaneously hypertensive rat (SHRSP), the Cl Ϫ component of dietary NaCl dominantly determines its pressor effect (salt-sensitivity). We telemetrically measured systolic aortic blood pressure (SBP) in SHRSP loaded with: nothing (CTL); NaCl alone (NaCl) (44 mmol/100 grams chow); KCl (KCl) alone (44 mmol); NaCl (44 mmol) combined with KHCO 3 (77 mmol) (NaCl/KBC) or with KCl (77 mmol) (NaCl/KCl). Across all groups, from age 10 to 15 or 16 weeks, SBP increased linearly (mm Hg/week) (dp/dt, change in SBP as a function of time): CTL, 5.6; NaCl, 9.5; KCl, 8.8; NaCl/KBC, 9.1; and NaCl/KCl, 14.6. Thus, the value of dp/dt in KCl matched that in NaCl. The value of dp/dt in NaCl/KCl exceeded that in NaCl in direct proportion to the greater Cl Ϫ load. Across all groups, only Cl Ϫ load bore a direct, highly linear relationship with dp/dt. Strokes occurred only, but always with SBP Ͼ250 mm Hg, a value observed almost exclusively in NaCl/KCl. Thus, Cl Ϫ dominantly determined the pressor effect induced with dietary NaCl, both with NaCl loaded alone and combined with either KCl or KHCO 3 , and thereby likely determined the occurrence of stroke with NaCl loading. Over the initial 3-day period of NaCl loading and exacerbating hypertension, external balance of Na ϩ increased similarly among all groups. However, within 24 hours of initiating NaCl loading, urinary creatinine excretion decreased in direct proportion to dp/dt and urinary Cl Ϫ excretion. We conclude that in the SHRSP, the Cl Ϫ component of a dietary NaCl dominantly determines salt sensitivity and thereby phenotypic expression. We suggest that Cl

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Alterations in renal vascular resistance and reactivity in spontaneous hypertension of rats

Cited by 54 publications

References 0 publications

Sympathetic Regulation of the Renal Functions in Rats Reciprocally Congenic for Chromosome 1 Blood Pressure Quantitative Trait Locus

Sympathetic Regulation of the Renal Functions in Rats Reciprocally Congenic for Chromosome 1 Blood Pressure Quantitative Trait Locus

Enhanced vascular tone in the renal vasculature of spontaneously hypertensive rats.

Chloride-Dominant Salt Sensitivity in the Stroke-Prone Spontaneously Hypertensive Rat

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