Sekihara H
Endocrinology. 1983 Sep;113(3):1141-8. doi: 10.1210/endo-113-3-1141.
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.
我们曾基于对肾上腺切除大鼠进行生物测定所获结果，将19 - 羟基雄烯二酮（19 - OH - A - 二酮）报告为醛固酮作用的增强剂。本研究对有肾上腺的大鼠评估了其生物活性。给大鼠施用19 - OH - A - 二酮会导致钠潴留、高血压、肾素活性受抑制以及血浆醛固酮、皮质酮和脱氧皮质酮浓度降低。19 - OH - A - 二酮的钠潴留和致高血压作用比醋酸脱氧皮质酮更强。螺内酯可抑制19 - OH - A - 二酮的作用。结果表明，19 - OH - A - 二酮虽缺乏盐皮质激素活性，但在肾上腺皮质存在的情况下，作为一种强效的钠潴留剂发挥作用，并引发类似盐皮质激素过多的高血压状态。
