Horiuchi T, Tanaka K, Shimizu N
Life Sci. 1987 Jun 22;40(25):2421-8. doi: 10.1016/0024-3205(87)90757-0.
Effect of adrenergic activity on the adrenal steroidogenesis and the modulation by catecholamines of aldosterone release were studied in isolated rat adrenal cell suspensions. Isoproterenol, norepinephrine and epinephrine, but not dopamine, caused statistically significant increase in aldosterone release. Both prazosin (alpha 1 antagonist) and yohimbine (alpha 2 antagonist) suppressed the norepinephrine-induced aldosterone release in a dose dependent manner, respectively. Both atenolol (beta 1 antagonist) and ICI 118-551 (beta 2 antagonist) also blocked (-)-isoproterenol-induced aldosterone release in a dose dependent manner, respectively. Neither (-)-isoproterenol nor (+/-)-norepinephrine at concentrations of 10(-6) M potentiated aldosterone release stimulated by angiotensin II or ACTH. These results suggest that catecholamines stimulate aldosteroidogenesis, but it appears unlikely that aldosterone release induced by ACTH or angiotensin-II is modulated by adrenergic stimulation.
在分离的大鼠肾上腺细胞悬液中研究了肾上腺素能活性对肾上腺类固醇生成的影响以及儿茶酚胺对醛固酮释放的调节作用。异丙肾上腺素、去甲肾上腺素和肾上腺素（而非多巴胺）可使醛固酮释放量出现具有统计学意义的增加。哌唑嗪（α1拮抗剂）和育亨宾（α2拮抗剂）均分别以剂量依赖的方式抑制去甲肾上腺素诱导的醛固酮释放。阿替洛尔（β1拮抗剂）和ICI 118 - 551（β2拮抗剂）也分别以剂量依赖的方式阻断（-）-异丙肾上腺素诱导的醛固酮释放。浓度为10^(-6) M的（-）-异丙肾上腺素或（±）-去甲肾上腺素均未增强血管紧张素II或促肾上腺皮质激素刺激的醛固酮释放。这些结果表明，儿茶酚胺可刺激醛固酮生成，但促肾上腺皮质激素或血管紧张素II诱导的醛固酮释放似乎不太可能受到肾上腺素能刺激的调节。
