Spontaneously Hypertensive Rats

نویسندگان

  • Graham P. McLennan
  • Robert L. Kline
  • Paul F. Mercer
چکیده

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 mgkg"'day"' 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 jtl-kg~'-min~') containing high levels of aldosterone, arginine vasopressin, 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), enalapriltreated 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 n are not the primary reason for the difference in the pressure-natriuresis relation in control Wistar-Kyoto and spontaneously hypertensive rats in this preparation. (Hypertension 1991;17:54-62)

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تاریخ انتشار 2005