Abstract
The hypertensinogenic effects of 19-hydroxyandrostenedione (19-OH-A-dione), which we reported as an amplifier of the action of aldosterone on the basis of the results obtained in bioassays using adrenalectomized rats, were evaluated in intact rats with both adrenals and kidneys. The administration of 19-OH-A-dione to the rats caused sodium retention and the 19-OH-A-dione treated rats developed high blood pressure, suppressed plasma renin activity and low plasma aldosterone, corticosterone and deoxycorticosterone concentrations. The hypertensinogenic potency of 19-OH-A-dione was incomparably higher than that of DOC A. The results indicate that 19-OH-A-dione is a potent hypertensinogenic steroid and causes the hypertensive state similar to mineralocorticoid excess. The evaluation of 19-OH-A-dione concentrations in human plasma revealed that 19-OH-A-dione is present in human peripheral circulation. It appears to be secreted by the adrenal cortex under the control of ACTH and the renin-angiotensin system. Plasma 19-OH-A-dione concentrations in patients with normal renin essential hypertension and low renin essential hypertension are higher than those in control subjects. 19-OH-A-dione is a newly recognised hypertensinogenic steroid in man.
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