Studies of the Pathogenesis of Human Hypertension

Abstract

Studies done in our laboratory have established definite abnormalities of adrenocortical activity in hypertensive patients as compared to normal subjects; (1) a significant ("P" < 0.001) mean increase in urinary aldosterone in all groups of hypertensive patients (essential, renal and malignant). (2) excessive daily fluctuations of urinary aldosterone in benign and severe hypertensive patients. (3) a significant ("P" 0.001) mean decrease in urinary pregnanetriol. (4) a urinary pregnanetriol/ aldosterone ratio below the lower limit of normal range in 92% of hypertensive patients. A direct relationship between the kidneys, the adrenal cortex and sodium was shown (a) by the finding of a marked and quite specific stimulation of urinary aldosterone during and after administration of Valine-5 angiotensin n, aspartic B-amide infused intravenously at hypertensive rates (i.e., with an increase of 15 to 35 mm Hg in diastolic pressure above control levels). Similar findings, although less marked, were obtained during infusions of angiotensin given at sub-hypertensive rates (i.e. without any significant rise in diastolic pressure). The increased aldosteronuria was accompanied by marked sodium retention and fall in urinary Na/K ratio in normal subjects, whereas hypertensive patients responded by a profuse natriuresis and an increase in Na/K ratio, (b) By the demonstration of the presence of angiotensin in the blood of some hypertensive patients, with the help of a new procedure for its isolation and determination. (Can. Jour. Biochem. and Physiol. 39: 581, 1961.).