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pubmed:abstractText |
The hypertensiogenic effects of 19-hydroxyandrostenedione (19-OH-A-dione) reported previously to be an amplifier of the action of aldosterone were evaluated using the same experimental procedures as for DOCA-salt hypertension in rats. The 19-OH-A-dione treated rats developed high blood pressure, hypokalemia, suppressed plasma renin activity and low plasma aldosterone and corticosterone concentrations as the DOCA treated rats did. The results demonstrate that 19-OH-A-dione amplifies the action of endogenous aldosterone and causes a hypertensive state simulating mineralocorticoid excess. Amplifiers of the action of aldosterone are considered to work as hypertensinogenic agents in the presence of the adrenal cortex.
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