EFFECT OF ENALAPRIL TREATMENT ON THE PRESSURE NATRIURESIS CURVE IN SPONTANEOUSLY HYPERTENSIVE RATS

The effect of chronic angiotensin I converting enzyme inhibition on the pressure-natriuresis relation was studied in Wistar-Kyoto and spontaneously hypertensive rats. Enalapril maleate (25 mg.kg-1.day-1 in drinking water) was started at 4-5 weeks of age. At 7-9 weeks of age, the pressure-natriuresis relation was studied while the rats were under Inactin anesthesia 1 week after the right kidney and adrenal gland were removed. Neural and hormonal influences on the remaining kidney were fixed by surgical renal denervation, adrenalectomy, and infusion of a hormone cocktail (330 mu-l.kg-1.min-1) containing high levels of aldosterone, arginine vasopressin, sin, hydrocortisone, and norepinephrine dissolved in 0.9% NaCl containing 1% albumin. Changes in renal function resulting from alterations in renal artery pressure were compared between enalapril-treated and control rats. Mean arterial pressure (+/-SEM) under anesthesia was 118+/-5, 94+/-4, 175+/-3, and 124+/-2 mm Hg for control Wistar-Kyoto (n = 10), enalapril-treated Wistar-Kyoto (n = 10), control spontaneously hypertensive (n = 9), and enalapril-treated spontaneously hypertensive (n = 9) rats, respectively. When renal artery pressure was set at values above approximately 125 mm Hg, control spontaneously hypertensive rats excreted less sodium and water than control Wistar-Kyoto rats. Enalapril treatment resulted in a significant and similar shift to the left of the pressure-natriuresis relation in both strains of rats so that a lower renal artery pressure was required to excrete a similar amount of sodium when compared with their respective untreated controls. Over the pressure range where differences in the pressure-natriuresis relation were significant, both renal blood flow and glomerular filtration rate were autoregulated and similar in all four groups. The similar effect of enalapril on the pressure-natriuresis curve in Wistar-Kyoto and spontaneously hypertensive rats suggests that the renal effects of angiotensin II are not the primary reason for the difference in the pressure-natriuresis relation in control Wistar-Kyoto and spontaneously hypertensive rats in this preparation.