Abnormal pressure-diuresis-natriuresis response in spontaneously hypertensive rats

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Abstract
The renal responses to changes in perfusion pressure (RPP) were studied in spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) to determine whether an abnormality in the pressure-diuresis phenomenon could be involved in the resetting of kidney function in hypertension. Differences in the neural and endocrine background to the kidneys were minimized by denervating the kidney and by holding plasma vasopressin, aldosterone, corticosterone and norepinephrine levels constant by i.v. infusion. In WKY, increasing renal perfusion pressure 54 mmHg, from 103-157 mm Hg, produced a 9-fold increase in urine flow and Na excretion with no measurable change in renal blood flow (RBF) or glomerular filtration (GFR). In SHR, increasing renal perfusion pressure 54 mm Hg, from 133-187 mm Hg, produced only a 4-fold increase in urine flow and Na excretion. GFR, RBF and peritubular capillary pressures were well autoregulated and were similar in the SHR and WKY at pressures > 110 mm Hg. Apparently, there are intrinsic changes in the kidney of SHR that enhance fractional tubular reabsorption and impair the pressure-diuresis response. This blunting of the renal pressure-diuresis phenomenon in SHR may represent the functional resetting of the kidney that is necessary for sustained hypertension.