Renal and nephron hemodynamics in spontaneously hypertensive rats

Arendshorst, William J.; Beierwaltes, W. H.

doi:10.1152/ajprenal.1979.236.3.f246

Cited by 112 publications

(103 citation statements)

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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: 57%

“…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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confidence: 99%

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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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Section: Altered Pressure Response Of the Interiobular Artery In Sponmentioning

confidence: 57%

mentioning

confidence: 99%

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

1992

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“…Hemodynamic changes in the kidney, eg, increased vascular resistance, 15 during the development of hypertension might also contribute to altered oxygen tension in the kidney.…”

Section: Discussionmentioning

confidence: 99%

Increased Kidney Xanthine Oxidoreductase Activity in Salt-Induced Experimental Hypertension

et al. 1998

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Abstract-Clinical and experimental studies have established an association between high sodium intake and arterial hypertension. The renal mechanisms resulting in impaired sodium excretion in hypertension-prone subjects are not clear. In hypertension-prone rats, high blood pressure results in increased renal mass and hemodynamic changes, both of which may alter renal oxygen distribution. Xanthine oxidoreductase (XOR) oxidizes ATP metabolites hypoxanthine and xanthine to urate. Because XOR is induced by hypoxia, we assessed kidney XOR activity in 2 models of salt-sensitive hypertension, spontaneously hypertensive rats (SHR) and Dahl salt-sensitive (Dahl S) rats. Increasing sodium intake from basal (0.08%) to high (2.56% wt/dry wt in the diet) increased renal XOR activity dose-dependently from 68Ϯ8 to 143Ϯ21 U/mg protein in the Dahl S (PϽ0.05) but not in Dahl salt-resistant (Dahl R) rats. On basal and high sodium diets, SHR had higher renal XOR activity (101Ϯ10 and 134Ϯ26 U/mg protein, respectively) than normotensive Wistar-Kyoto rats (55Ϯ2 and 58Ϯ6 U/mg protein, PϽ0.05). Sodium restriction (0.02% wt/wt) downregulated kidney XOR activity in both Dahl S and R rats by nearly 40%. In SHR, allopurinol treatment totally inhibited renal XOR activity, but neither systolic blood pressure nor renal mass changed. The results suggest that renal XOR induction is a consequence of increased salt intake or the resulting hypertension. However, further studies on renal XOR activity during the development of hypertension are needed to assess the importance of XOR in the pathophysiology of arterial hypertension. (Hypertension. 1998;32:902-906.)Key Words: hypertension, essential Ⅲ xanthine oxidoreductase Ⅲ rats, inbred SHR Ⅲ rats, Dahl Ⅲ hypertrophy Ⅲ sodium Ⅲ allopurinol I n salt-sensitive rats, increasing salt intake results in marked hypertension and left ventricular and renal enlargement within weeks. The genetically related salt-insensitive rats develop these harmful, sodium-induced effects to a much lesser extent.1-3 Kidney transplants derived from normotensive rats have been shown to decrease permanently the systolic blood pressure of an adult salt-sensitive recipient and also abolish the predisposition to hypertension in young animals.4,5 These observations, based on studies on the spontaneously hypertensive rat (SHR) and its normotensive control Wistar-Kyoto rat (WKY) as well as the Dahl saltsensitive (Dahl S) and salt-resistant (Dahl R) rat, indicate the crucial importance of the kidney in the pathogenesis of hypertension. Mechanisms resulting in an impaired excretion of sodium in relation to renal perfusion pressure in saltsensitive rat strains have not been fully worked out.

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“…32,33 The increase in resistance appears to be more marked in the renal vasculature compared with the increase seen in other vascular beds. 29 As renal resistance resides predominantly within the afferent arterioles, 34 the increased renal resistance could be caused by narrowing of the afferent arteriolar lumen. Indeed, morphometric studies on the afferent arteriole of SHR and WKY have confirmed that afferent arteriolar diameters are smaller in SHR compared with WKY, whereas efferent arteriole diameters are comparable between the two strains.…”

Section: Role Of the Renal Microvascular Remodeling In The Pathogenesmentioning

confidence: 99%

Prevention and regression of hypertension: role of renal microvascular protection

et al. 2009

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Hypertension is a disease which affects over 26.4% of the world adult population, therefore novel approaches to the prevention and treatment of this disease need to be examined. Previous studies from our and other laboratories have shown that treatment of spontaneously hypertensive rats (SHR) and Dahl salt-sensitive rats with a renin-angiotensin system (RAS) inhibitor during the 'critical period' in hypertension development results in prevention of the later development of hypertension. In humans, Julius et al. reported similar findings in the landmark TROPHY study. Recently, we reported that 'pulse' treatment of SHR with highdose angiotensin receptor blocker (ARB) is effective in causing sustained reduction of already established hypertension, even when the treatment was started after the 'critical period'. These results suggest the possibility that 'regression' of established hypertension may become feasible, and we have started a prospective, multicenter clinical study (STAR CAST study) to examine this possibility. In our animal studies, we found that treatment of rats during the 'critical period' with an ARB inhibits the development of renal arteriolar hypertrophy. Moreover, a high-dose angiotensin blocker caused a remarkable reversal of renal arteriolar hypertrophy in SHR, which was associated with changes in microvascular MMP expression. These results suggest that changes in the renal microvasculature may have an important role in the mechanisms of hypertension prevention and regression by ARB.

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Renal and nephron hemodynamics in spontaneously hypertensive rats

Cited by 112 publications

References 0 publications

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

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

Increased Kidney Xanthine Oxidoreductase Activity in Salt-Induced Experimental Hypertension

Prevention and regression of hypertension: role of renal microvascular protection

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