Development of hypertension in rats treated with aldosterone acetate

Abstract

Chronic (10 week) administration of graded doses of d-aldosterone acetate (10, 20, or 40 μg/day) to unilaterally nephrectomized, saline-treated rats increased both their systolic blood pressure and heart weight above the level observed for controls. Thus, doses of aldosterone within the physiological range (2–25 μg/100 g body weight per day) can induce hypertension in “sensitized” rats. Administration of the same doses for the same length of time to intact rats in a second experiment induced smaller rises in blood pressure and no significant cardiac hypertrophy. A sigmoid relationship was observed between the ratio of thyroid weight to body weight and arbitrary ranges of systolic blood pressure for all rats to which aldosterone was administered chronically. Thyroid weight ratio first increased significantly when systolic blood pressure rose to levels of 160–169 mm Hg. The maximal increase in thyroid weight was 25–30% above that of untreated controls. The sigmoid relationship suggests that an unidentified, primary factor elevates blood pressure to the threshold range without thyroid mediation but when the threshold range of blood pressure is exceeded, thyroid weight increases and may mediate further elevation of blood pressure. Hence, the thyroid gland may play a secondary role in the development of aldosterone-induced hypertension. Administration of 1.1 μg d-aldosterone acetate/100 g body weight per day had no effect on the elevated blood pressure of rats whose kidneys were bilaterally encapsulated with latex envelopes. However, administration of 3.0 μg d-aldosterone acetate/100 g body weight per day to rats whose kidneys were recently bilaterally encapsulated with latex envelopes accelerated the rate of elevation of systolic blood pressure. Thus, small doses of aldosterone can accelerate the development of renal hypertension in rats.