Abnormalities in glomerular function in rats developing spontaneous hypertension

Dilley, J. R.; Stier, Charles T.; Arendshorst, William J.

doi:10.1152/ajprenal.1984.246.1.f12

Cited by 81 publications

(86 citation statements)

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“…This finding differs from those of Dilley and colleagues 27 n and others, 29 who reported that GFR and RBF were markedly reduced in 6-to 9-week-old euvolemic SHR compared with WKY. They suggested that the renal vasoconstriction in the SHR was due to an enhanced tubuloglomerular feedback response.…”

contrasting

confidence: 98%

Renal cortical and papillary blood flow in spontaneously hypertensive rats.

Roman

Kaldunski

1988

Hypertension

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SUMMARY The present study examined whether an alteration in renal medullary hemodynamics is associated with the development of hypertension in the spontaneously hypertensive rat (SHR). The relationships between whole kidney, cortical and papillary blood flows, and renal perfusion pressure were compared in 3-to 5-, 6-to 9-, and 12-to 16-week-old SHR and Wistar-Kyoto rats (WKY). Cortical and papillary blood flows were measured using a laser-Doppler flowmeter. Whole kidney and superficial cortical blood flows were similar in the different age groups of SHR and WKY over most of the range of perfusion pressure studied. Control papillary blood flows, determined at a renal perfusion pressure equal to the mean arterial pressure of each animal, were not significantly different in the 3-to 5-and 12->to 16-week-old SHR in comparison to values observed in age-matched WKY. In contrast, the control papillary blood flow was 30% lower in 6-to 9-week-old SHR in comparison to the value observed in WKY. Papillary blood flows were significantly less in all age groups of SHR than the corresponding flows measured in WKY when they were compared at equivalent renal perfusion pressures. These findings indicate that medullary vascular resistance is elevated even in very young SHR and suggest that alterations in vasa recta hemodynamics may participate in the development of hypertension by shifting the pressure-natriuresis relationship toward higher pressures. 1 -2 The kidneys of hypertensive patients 3 and genetically hypertensive rats 4 " 6 require an elevated renal perfusion pressure (RPP) to excrete sodium and water normally. We have demonstrated that the pressure-natriuresis relationship is shifted toward higher pressures even in very young, 3-to 5-week-old SHR. 6 The factors responsible for resetting the pressure-natriuresis relationship in this model of hypertension are unknown.Recent studies have indicated that elevations in RPP increase the delivery of sodium to the tip of the loop of Henle 7 and that chemical papillectomy blunts the pres- sure-natriuretic response. 8 These findings indicate that inhibition of tubular reabsorption in the deep nephrons contributes to the pressure-natriuretic response. Moreover, our studies indicating that elevations in RPP increase pressure and flow in the renal vasa recta circulation suggest that changes in medullary hemodynamics may signal the pressure-natriuresis response.9 "" The present study examined whether an alteration in renal medullary hemodynamics is associated with the development of hypertension in the SHR. The relationships between renal blood flow (RBF), cortical and papillary blood flows, and RPP were compared in 3-to 5-, 6-to 9-, and 12-to 16-week-old SHR and WistarKyoto rats (WKY). The results indicate that renal medullary vascular resistance is elevated early in the development of hypertension and suggest that changes in medullary hemodynamics may participate in the resetting of the pressure-natriuresis relationship in the SHR. Materials and MethodsExperiments were performed on ...

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confidence: 98%

Renal cortical and papillary blood flow in spontaneously hypertensive rats.

Roman

Kaldunski

1988

Hypertension

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“…6 -7 ' 20 The results of the present study indicate that the intermediate ILA segment exhibits an augmented myogenic response that may also contribute to the increased preglomerular resistance, especially of superficial glomeruli. It is tempting to speculate that the enhanced vasoconstriction of the intermediate ILA acts in concert with afferent arteriolar vasoconstriction to prevent or attenuate elevated glomerular capillary pressure in superficial nephrons.…”

Section: Altered Pressure Response Of the Interiobular Artery In Sponmentioning

confidence: 61%

Enhanced myogenic responsiveness of renal interlobular arteries in spontaneously hypertensive rats.

1992

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We recently demonstrated that the interlobular artery (ILA) constricts in response to elevating renal arterial pressure (RAP), suggesting that the ILA contributes to renal autoregulation. In the present study, we examined the segmental myogenic responsiveness of the ILA in kidneys from Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR). The tapered nature of the ILA allowed us to characterize the regional responsiveness, using the basal diameter to define segments as either proximal (greater than 60 fim), intermediate ( 2 We have previously demonstrated that myogenic afferent arteriolar vasoconstriction is reset to higher renal arterial pressure (RAP) levels in spontaneously hypertensive rats (SHR).3 Although the afferent arteriole is primarily responsible for both acute 4 -5 and chronic 6 ' 7 adaptations to elevated RAP, the interlobular artery (ILA) may also contribute to renal autoregulation. 8 ' 9 The involvement of the ILA in chronic adaptations of the renal vasculature to hypertension has not been previously examined.

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“…34 -36 A lower whole kidney glomerular filtration rate has also been reported in SHR during the a. development of hypertension. 37 All this accumulated evidence suggests that abnormalities in renal function may be involved in the pathogenesis of hypertension in SHR, more so when kidneys transplanted from SHR into Fl hybrids significantly raise blood pressure in the latter. 38 SHR are known to respond with exaggerated natriuresis when challenged with an acute sodium load 353940 ; however, this response is abolished when renal perfusion pressure is acutely reduced to normotensive levels, 40 -42 mainly through a decrease in the glomerular filtration rate.…”

Section: Discussionmentioning

confidence: 99%

Glomerular atrial natriuretic factor receptors in spontaneously hypertensive rats.

et al. 1989

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There are differences in the renal handling of sodium between spontaneously hypertensive rats (SHR) and their normotensive controls. We investigated whether this difference may be associated with changes in plasma and tissue atrial natriuretic factor (ANF) levels and with alterations in glomerular ANF receptors at 4, 8, 12, and 16 weeks of age. Age-matched Wistar-Kyoto (WKY) and Wistar rats were used as normotensive controls. Systolic blood pressure was higher in SHR at 8, 12, and 16 weeks, and cardiac hypertrophy was also present in these animals at 4 weeks. Plasma ANF C-and N-terminal concentrations were greater than in both normotensive groups at 8 and 16 weeks. ANF in the right atrium was higher in SHR than in WKY rats and identical to that in the Wistar group at 4 and 8 weeks. ANF in the left atrium was lower in SHR than in both control groups at week 12. No differences were found in ventricular ANF content. The density of glomerular ANF binding sites increased with age in WKY and Wistar rats but not in SHR. At weeks 8, 12, and 16, both normotensive groups had a higher density of binding sites than SHR, but binding site affinity was greater in SHR at weeks 8 and 12. After incubation with increasing concentrations of ANF, the production of cyclic guanosine monophosphate (cGMP) by isolated glomeruli from 16-week-old rats was lower in SHR than in both normotensive groups. We conclude that the development of hypertension in SHR is associated with higher plasma ANF levels and decreased glomerular ANF receptor density and glomerular cGMP production. Through modulation of ANF glomerular receptors, ANF in SHR, when compared with normotensive counterparts, may contribute to the difference in renal sodium handling. (Hypertension 1989; 13:567-574)

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Abnormalities in glomerular function in rats developing spontaneous hypertension

Cited by 81 publications

References 0 publications

Renal cortical and papillary blood flow in spontaneously hypertensive rats.

Renal cortical and papillary blood flow in spontaneously hypertensive rats.

Enhanced myogenic responsiveness of renal interlobular arteries in spontaneously hypertensive rats.

Glomerular atrial natriuretic factor receptors in spontaneously hypertensive rats.

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