Melby J C, Dale S L
Am J Cardiol. 1976 Nov 23;38(6):805-13. doi: 10.1016/0002-9149(76)90359-3.
Alterations in steroidogenesis have been demonstrated in experimental and human hypertension. It is highly likely that increased secretion of the nonaldosterone mineralocorticoid deoxycorticosterone (DOC) and 18-hydroxy-11-deoxycorticosterone (18-OH-DOC) may initiate or perpetuate hypertension, or both. It is possible that 16 beta-hydroxydehydroeplandrosterone (16beta-OH-DHEA) directly induces the hypertensive process in animals. The significance of the findings of increased secretion of 16 alpha, 18-dihydroxy-11-deoxycorticosterone (16alpha, 18-diOH-DOC) and dehydroepiandrosterone sulfate (DHEA-S) cannot now be appreciated. Neither has been examined experimentally for its ability to induce hypertension, and the former compound is not a mineralocorticoid. It does possess the curious property of increasing mineralocorticoid activity of other steroids, by altering either their metabolism or mode of action. Variations in the mineralocorticoid hypertensive syndrome or, more aptly, the steroid hypertensive syndrome could account for the hypertension in a substantial portion of patients with reduced plasma renin activity.
在实验性高血压和人类高血压中均已证实存在类固醇生成的改变。非醛固酮类盐皮质激素脱氧皮质酮（DOC）和18-羟-11-脱氧皮质酮（18-OH-DOC）分泌增加极有可能引发高血压或使高血压持续存在，或两者皆有。16β-羟基脱氢表雄酮（16β-OH-DHEA）有可能直接在动物中诱发高血压过程。目前尚无法明确16α,18-二羟基-11-脱氧皮质酮（16α,18-二OH-DOC）和硫酸脱氢表雄酮（DHEA-S）分泌增加这一发现的意义。尚未对它们诱发高血压的能力进行实验研究，而且前一种化合物并非盐皮质激素。它确实具有一种奇特的特性，即通过改变其他类固醇的代谢或作用方式来增强其盐皮质激素活性。盐皮质激素性高血压综合征，或者更确切地说，类固醇性高血压综合征的变化，可能是血浆肾素活性降低的大部分患者出现高血压的原因。
