Yamakado M, Franco-Saenz R, Mulrow P J
Proc Soc Exp Biol Med. 1985 Jul;179(3):318-23. doi: 10.3181/00379727-179-42103.
The sites of action of beta-melanocyte stimulating hormone (beta-MSH) on aldosterone biosynthesis were studied using collagenase-dispersed adrenal glomerulosa cells from rats maintained on either normal or sodium-deficient diets for 2 weeks. Isolated cells were treated with a cyanoketone derivative (WIN 19,578) to isolate the early and late steps in aldosterone biosynthesis. WIN 19,578 (1 microM) completely blocked aldosterone production stimulated by sodium depletion, AII, ACTH, and beta-MSH. beta-MSH (1 microM) significantly stimulated pregnenolone production (early step) and the conversion of corticosterone to aldosterone (late step) in aldosterone biosynthesis. The effect of beta-MSH was similar to AII and ACTH. Sodium depletion enhanced the effect of beta-MSH only on the late step in aldosterone biosynthesis. In conclusion, beta-MSH stimulates both the early and late steps of aldosterone biosynthesis. These results suggest that beta-MSH or peptides containing beta-MSH may play a role in the regulation of aldosterone production.
使用胶原酶分散的肾上腺球状带细胞,研究了β-促黑素细胞激素(β-MSH)对醛固酮生物合成的作用位点,这些细胞取自正常饮食或缺钠饮食2周的大鼠。用氰基酮衍生物(WIN 19,578)处理分离的细胞,以分离醛固酮生物合成的早期和晚期步骤。WIN 19,578(1微摩尔)完全阻断了钠耗竭、血管紧张素II(AII)、促肾上腺皮质激素(ACTH)和β-MSH刺激的醛固酮生成。β-MSH(1微摩尔)显著刺激醛固酮生物合成中孕烯醇酮的生成(早期步骤)以及皮质酮向醛固酮的转化(晚期步骤)。β-MSH的作用与AII和ACTH相似。钠耗竭仅增强了β-MSH对醛固酮生物合成晚期步骤的作用。总之,β-MSH刺激醛固酮生物合成的早期和晚期步骤。这些结果表明,β-MSH或含β-MSH的肽可能在醛固酮生成的调节中起作用。