The Role of Aldosterone in the Development of Hypertension in Spontaneously Hypertensive Rats*

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Abstract
A continuous sc infusion of aldosterone for 2 weeks (10 μg/day) markedly increased the blood pressure of male, adrenalectomized (ADX), spontaneously hypertensive rats (SHR) from 142 to 178 mm Hg, which was similar to the increase seen in a group of sham-operated SHR. The blood pressure in a group of ADX SHR maintained without aldosterone declined from 141 to 119 mm Hg during the 2 weeks after surgery. Wistar Kyoto (WKY) and Sprague-Dawley (SD) rats treated in an identical fashion remained normotensive throughout. Adrenalectomy caused hyperkalemia in all strains of rat. Plasma potassium levels in aldosterone-treated WKY and SD rats were lower than those in sham-operated controls, but were similar to those in corresponding groups of SHR. Acute renal responses of ADX male rats showed that SHR reabsorbed more water and sodium of an injected isotonic saline load than WKY rats and excreted less potassium than either WKY or SD rats. Sensitivity to aldosterone in the three strains of rats was compared using the urinary sodium to creatinine and potassium to creatinine ratios 1-3 h postinjection of aldosterone. Decreases in the urinary ratio of sodium to creatinine in response to various doses of aldosterone (0-1.25 μg aldosterone) were similar for the three strains of rat. ADX SHR appeared to be less responsive to the kaliuretic actions of aldosterone than WKY and SD rats. The present studies show that aldosterone is essential to the development of hypertension in SHR. The hypertensinogenic actions of aldosterone in these rats may be related to a blunted kaliuretic response to mineralocorticoids.