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Hypertension, Vol 3, 67-74, Copyright © 1981 by American Heart Association

ARTICLES

Impaired renal blood flow and cortical pressure autoregulation in contralateral kidneys of Goldblatt hypertensive rats

DW Ploth, RN Roy, WC Huang and LG Navar

Experiments were conducted on two-kidney, one clip renal vascular hypertensive rats to assess the ability of the kidney contralateral to renal vascular stenosis to autoregulate renal blood flow (RBF), glomerular filtration rate (GFR), and hydrostatic pressures in cortical structures during conditions of acutely reduced renal arterial blood pressure (BP). When observed at their respective, spontaneous BPs, RBF and GFR were not different in the contralateral kidneys of the hypertensive rats (n = 11) compared to normal animals (n = 7). However, the contralateral kidneys exhibited a significantly higher renal vascular resistance (RVR), 28.9 +/- 2.8 mm Hg . min/ml than the control animals, 23.1 +/- 1.5 mm Hg . min/ml. At spontaneous BP (169 +/- 5 mm Hg), urine flow, absolute and fractional sodium excretion, and absolute and fractional potassium excretion were all significantly greater in the contralateral kidneys of hypertensive rats than in kidneys of normal rats. Hydrostatic pressures in cortical structures were similar in the two groups. When BP was reduced acutely, the kidney contralateral to the renal artery stenosis achieved only small decreases in RVR that failed to allow RBF, GFR, or cortical pressures to be maintained. In contrast, normal rats efficiently autoregulated RBF and GFR. In addition, hydrostatic pressures in proximal tubules, distal tubules, and first order peritubular capillaries were maintained during reductions in BP to as low as 100 mm Hg. Urine flow and electrolyte excretion decreased to a greater extent in the hypertensive kidneys, such that at comparable BP these indices of excretory function were not different in the two groups. These observations indicate that the capacity of the contralateral kidney to maintain hemodynamic and glomerular function at reduced BP is compromised severely and suggest the possibility that the impaired autoregulatory capability may contribute to the maintenance of hypertension observed in this model.

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