ALDOSTERONE AND CORTICOSTERONE PRODUCTION IN RENAL HYPERTENSIVE RATS

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Abstract
The development of hypertension, which had been elicited by clamping one renal artery in the presence of an untouched contralateral kidney, has been pursued in rats for up to six weeks after operation, and aldosterone and corticosterone production was studied at various intervals. Two weeks after renal artery stenosis had been induced, a "benign" and a "malignant" course of hypertension could be distinguished, the latter being characterized by a rise in blood pressure beyond 180–190 mmHg, loss of salt and water, increased water intake, decrease in body weight and food intake, and stimulation of the renin-angiotensin system. In the early phase of hypertension (after 9 days), aldosterone production and plasma aldosterone concentration were already elevated, and so was plasma corticosterone concentration. After 16 days, a marked increase in aldosterone production and in both plasma aldosterone and corticosterone concentrations was obtained in malignant hypertensive rats, whereas the secretion of the two hormones was only slightly stimulated in benign hypertensive rats. Similar differences in aldosterone production between rats with benign or malignant hypertension were found 21 and 42 days after operation. After 21 days, a close relationship between plasma renin concentration and aldosterone production was obtained in malignant hypertensive and control rats. A positive correlation between plasma concentrations of angiotensin II and of aldosterone was calculated for rats with malignant hypertension. It is concluded that, in the malignant phase of renal hypertension, a state of secondary aldosteronism develops as a consequence of negative sodium and water balance induced by high blood pressure.

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