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钾离子诱导培养的大鼠肾小球旁细胞中醛固酮的生物合成

Potassium-induced aldosterone biosynthesis in cultured rat zona glomerulosa cells.

作者信息

Müller J, Lauber M, Schmid C

机构信息

Department of Medicine, University Hospital, Zürich, Switzerland.

出版信息

Am J Physiol. 1989 Apr;256(4 Pt 1):E475-82. doi: 10.1152/ajpendo.1989.256.4.E475.

Abstract

Rat adrenal zona glomerulosa cells lost their ability to produce aldosterone from either endogenous precursors or added deoxycorticosterone within 2 days of primary monolayer culture in a medium with a potassium concentration of 6.3 mmol/l. The lost corticosterone methyl oxidase I and II activities were totally regenerated when the ambient potassium concentrations was raised to 31 mmol/l. The conversions of deoxycorticosterone to 18-hydroxycorticosterone and aldosterone were completely restored by culture in a high-potassium medium also in zona glomerulosa cells of rats in which aldosterone biosynthesis had been suppressed by potassium restriction and sodium loading. However, these conversions were not induced in zona fasciculata-reticularis cells. The induction of aldosterone biosynthesis was associated with the appearance of a mitochondrial 49,000 protein cross-reacting with an antibody raised against bovine adrenal cytochrome P-450(11) beta. Thus primary cultures of zona glomerulosa cells are promising models for studying in vitro the molecular mechanisms of long-term adaptation of aldosterone biosynthesis to sodium and potassium intake.

摘要

在钾浓度为6.3 mmol/l的培养基中进行原代单层培养的2天内,大鼠肾上腺球状带细胞丧失了从内源性前体或添加的脱氧皮质酮产生醛固酮的能力。当环境钾浓度升至31 mmol/l时,丧失的皮质酮甲基氧化酶I和II活性完全恢复。在高钾培养基中培养时,脱氧皮质酮向18-羟皮质酮和醛固酮的转化在因钾限制和钠负荷而使醛固酮生物合成受到抑制的大鼠球状带细胞中也完全恢复。然而,在束状带-网状带细胞中未诱导出这些转化。醛固酮生物合成的诱导与一种分子量为49000的线粒体蛋白的出现有关,该蛋白与针对牛肾上腺细胞色素P-450(11)β产生的抗体发生交叉反应。因此,球状带细胞的原代培养是在体外研究醛固酮生物合成对钠和钾摄入的长期适应性分子机制的有前景的模型。

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