Nakajima S, Suzuki H, Saito I, Saruta T
Acta Endocrinol (Copenh). 1987 May;115(1):57-62. doi: 10.1530/acta.0.1150057.
This study was undertaken to examine the effects of atrial natriuretic peptide (ANP), dopamine, and ouabain, which each are considered to be a kind of natriuretic factor, on aldosterone synthesis in vivo and in vitro. In the in vivo experiments, during infusion of one of the natriuretic factors, ANP (64 pmol X min-1 X kg-1), dopamine (20 nmol X min-1 X kg-1) or ouabain (684 II pmol x min-1 x kg-1), the stimulatory action of angiotensin (20 pmol X min-1 X kg-1) or adrenocorticotropin (ACTH, 7 pmol X min-1 X kg-1) on aldosterone synthesis was investigated in 36 anaesthetized (pentobarbital, 40 mg/kg, iv) female rabbits. In the basal condition, aldosterone synthesis was suppressed slightly by each of the natriuretic factors. The stimulatory actions of angiotensin II and ACTH on aldosterone synthesis were significantly attenuated by pre-treatment with ANP and dopamine. However, ouabain infusion did not induce any changes in the synthesis of aldosterone, 18-hydroxycorticosterone (18-OHB), and corticosterone (B) in either the basal or the stimulated conditions. For the in vitro experiments, rabbit adrenal glomerulosa cells (10(5) cells/tube) were used. The effects of ANP and dopamine on the aldosterone synthesis revealed results identical to those from the in vivo study. However, in contrast to the in vivo study, ouabain completely inhibited the synthesis of aldosterone, 18-OHB and B. The above results obtained in vivo and in vitro suggest that ANP inhibits corticosterone methyloxidase II activity and dopamine inhibits corticosterone methyloxidase I activity. However, from the present study we were unable to specify the action of ouabain on the synthesis of aldosterone and its related substances.
本研究旨在探讨心房利钠肽（ANP）、多巴胺和哇巴因（每一种都被认为是一种利钠因子）对体内和体外醛固酮合成的影响。在体内实验中，在输注一种利钠因子（ANP，64 pmol·min⁻¹·kg⁻¹；多巴胺，20 nmol·min⁻¹·kg⁻¹；或哇巴因，684 pmol·min⁻¹·kg⁻¹）期间，研究了血管紧张素（20 pmol·min⁻¹·kg⁻¹）或促肾上腺皮质激素（ACTH，7 pmol·min⁻¹·kg⁻¹）对36只麻醉（戊巴比妥，40 mg/kg，静脉注射）雌性家兔醛固酮合成的刺激作用。在基础状态下，每种利钠因子均轻微抑制醛固酮合成。ANP和多巴胺预处理可显著减弱血管紧张素II和ACTH对醛固酮合成的刺激作用。然而，在基础或刺激条件下，输注哇巴因均未引起醛固酮、18 - 羟皮质酮（18 - OHB）和皮质酮（B）合成的任何变化。在体外实验中，使用家兔肾上腺球状带细胞（10⁵个细胞/管）。ANP和多巴胺对醛固酮合成的影响与体内研究结果一致。然而，与体内研究不同的是，哇巴因完全抑制了醛固酮、18 - OHB和B的合成。上述体内和体外实验结果表明，ANP抑制皮质酮甲基氧化酶II的活性，多巴胺抑制皮质酮甲基氧化酶I的活性。然而，从本研究中我们无法明确哇巴因对醛固酮及其相关物质合成的作用。
