19-Hydroxyandrostenedione: evidence for a new class of sodium-retaining and hypertensinogenic steroids.
The biological activities 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 rats with the adrenals. The administration of 19-OH-A-dione to the rats caused sodium retention, high blood pressure, suppressed PRA and low plasma aldosterone, corticosterone, and deoxycorticosterone concentrations. The sodium-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. The results indicate that 19-OH-A-dione, although it is devoid of mineralocorticoid activity, works as a potent sodium-retaining agent and causes a hypertensive state simulating mineralocorticoid excess in the presence of the adrenal cortex.
D000450:Aldosterone / Q000097:blood; D000735:Androstenedione / Q000031:analogs & derivatives* / Q000494:pharmacology; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects*; D003345:Corticosterone / Q000097:blood; D003900:Desoxycorticosterone / Q000097:blood / Q000494:pharmacology; D004347:Drug Interactions; D011188:Potassium / Q000378:metabolism; D051381:Rats; D012083:Renin / Q000097:blood; D012964:Sodium / Q000378:metabolism*; D013148:Spironolactone / Q000494:pharmacology
D013148:Spironolactone; D000735:Androstenedione; D003900:Desoxycorticosterone; D000450:Aldosterone; D012964:Sodium; C011482:19-hydroxy-4-androstene-3,17-dione; D012083:Renin; D011188:Potassium; D003345:Corticosterone