Sekihara H
Clin Exp Hypertens A. 1983;5(1):1-9. doi: 10.3109/10641968309048805.
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.
我们曾根据对肾上腺切除大鼠进行生物测定所得结果,报道6β-羟基雄烯二酮(6β-OH-A-二酮)是醛固酮促尿钾排泄作用的增强剂。本文对有肾上腺的大鼠评估了其致高血压作用,并与醛固酮保钠作用增强剂19-羟基雄烯二酮(19-OH-A-二酮)进行了比较。给有肾上腺的大鼠注射6β-OH-A-二酮会像注射19-OH-A-二酮一样引起钠潴留,并且6β-OH-A-二酮处理的大鼠会像19-OH-A-二酮处理的大鼠一样出现高血压、血浆肾素活性受抑制以及血浆醛固酮、皮质酮和11-脱氧皮质酮浓度降低。结果表明,6β-OH-A-二酮在肾上腺皮质存在的情况下作为一种致高血压剂起作用,并导致模拟盐皮质激素过多的高血压状态。本文进一步证明了醛固酮作用增强剂的致高血压作用,并提示醛固酮作用增强剂在人类高血压病因学中的重要性。