Abstract
The biological activities of 19-hydroxyandrostenedione (19-OH-A-dione), which was reported as an amplifier of the action of aldosterone on the basis of the results obtained in bioassays using adrenalectomized rats, were evaluated in rats with the adrenals. The administration of 19-OH-A-dione to the rats caused Na retention, high blood pressure, suppressed plasma renin activity and low plasma aldosterone, corticosterone, and deoxycorticosterone concentrations. The Na-retaining and hypertensinogenic effects of 19-OH-A-dione were more potent than those of deoxycorticosterone acetate. Spironolactone inhibited the action of 19-OH-A-dione. Although it is devoid of mineralocorticoid activity, 19-OH-A-dione works as a potent Na-retaining agent and causes a hypertensive state simulating mineralocorticoid excess in the presence of the adrenal cortex.