日粮钠、钾摄取量变化及代谢性酸中毒对大鼠肾脏11β -羟基类固醇脱氢酶活性的影响

A Thompson, M A Bailey, A E Michael, R J Unwin
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引用次数: 23

摘要

背景/目的:糖皮质激素活性受11β -羟基类固醇脱氢酶(11betaHSD)的NADP(+)-和NAD(+)依赖性同工型的调节,该酶将糖皮质激素转化为其无活性代谢物。NAD(+)依赖性异构体11betaHSD2存在于远端肾元中,在那里它赋予醛固酮对矿物皮质激素受体的特异性。本研究的目的是确定肾11β - ahsd活性是否受到钠钾平衡变化和代谢性酸中毒的影响。方法:分别饲喂正常、高、低钾日粮和低钠日粮或1.5% NH(4)Cl饮水的大鼠,体外测定肾脏11β - ahsd活性。结果:维持高钾低钠饮食的大鼠NAD(+)依赖性肾11β - ahsd活性(相对于对照组大鼠)分别下降59% (p < 0.01)和28% (p < 0.05), NADP(+)依赖性皮质醇氧化无变化。短期(3天)和长期(10天)代谢性酸中毒也使NAD(+)依赖性11betaHSD活性分别降低50%和52%,而不影响NADP(+)依赖性皮质醇氧化。低钾饮食对肾脏11β - ahsd活性无明显影响。结论:这些结果表明,适应高钾或低钠饮食以及代谢性酸中毒与肾11β - sd2活性降低有关,从而增加了糖皮质激素对肾皮质类固醇受体的通路。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Effects of changes in dietary intake of sodium and potassium and of metabolic acidosis on 11beta-hydroxysteroid dehydrogenase activities in rat kidney.

Background/aim: Glucocorticoid activity is modulated by NADP(+)- and NAD(+)-dependent isoforms of the enzyme 11beta-hydroxysteroid dehydrogenase (11betaHSD) which convert glucocorticoids to their inactive metabolites. The NAD(+)-dependent isoform, 11betaHSD2, is present in the distal nephron where it confers aldosterone specificity on mineralocorticoid receptors. The objective of this study was to establish whether renal 11betaHSD activities are affected by changes in sodium and potassium balance and by metabolic acidosis.

Methods: Renal 11betaHSD activities were measured ex vivo from rats fed normal and high- and low-potassium diets and a low-sodium diet or given 1.5% NH(4)Cl to drink.

Results: Rats maintained on high-potassium and low-sodium diets exhibited 59% (p < 0.01) and 28% (p < 0.05) decreases, respectively, in NAD(+)-dependent renal 11betaHSD activity (relative to rats fed control diet) with no changes in NADP(+)-dependent cortisol oxidation. Short-term (3 day) and longer-term (10 day) metabolic acidosis also decreased NAD(+)-dependent 11betaHSD activity by 50 and 52%, respectively, without affecting NADP(+)-dependent cortisol oxidation. The low-potassium diet had no detectable effect on renal 11betaHSD activities.

Conclusion: These results suggest that adaptations to a high-potassium or a low-sodium diet and to metabolic acidosis involve decreases in renal 11betaHSD2 activity, enhancing the access of glucocorticoids to renal corticosteroid receptors.

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