angiotensinogen and 19-hydroxy-4-androstene-3-17-dione

The hypertensinogenic effects of 6 beta-hydroxyandrostenedione (6 beta-OH-A-dione), which we reported as an amplifier of the kaliuretic action of aldosterone on the basis of the results obtained in bioassays using adrenalectomized rats, were evaluated in rats with the adrenals and compared with those of 19-hydroxyandrostenedione (19-OH-A-dione), an amplifier of the sodium-retaining action of aldosterone. The administration of 6 beta-OH-A-dione to rats with the adrenals caused sodium-retention as the administration of 19-OH-A-dione did and the 6 beta-OH-A-dione treated rats developed high blood pressure, suppressed plasma renin activity and low plasma aldosterone, corticosterone and 11-deoxycorticosterone concentrations as the 19-OH-A-dione treated rats did. The results demonstrate that 6 beta-OH-A-dione works as a hypertensinogenic agent in the presence of the adrenal cortex and causes the hypertensive state simulating mineralocorticoid excess. The present paper adds further evidence for the hypertensinogenic effects of amplifiers of the action of aldosterone and suggests the importance of amplifiers of the action of aldosterone in the etiology of human hypertension.

Topics: Aldosterone; Androstenedione; Angiotensinogen; Angiotensins; Animals; Corticosterone; Hypertension; Male; Potassium; Rats; Rats, Inbred Strains; Renin; Sodium