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钾作为胰岛素与肾素-血管紧张素-醛固酮系统之间的联系。

Potassium as a link between insulin and the renin-angiotensin-aldosterone system.

作者信息

Ferrannini E, Galvan A Q, Santoro D, Natali A

机构信息

CNR Institute of Clinical Physiology, University of Pisa, Italy.

出版信息

J Hypertens Suppl. 1992 Apr;10(1):S5-10. doi: 10.1097/00004872-199204001-00002.

Abstract

PURPOSE

To focus on the interactions between insulin secretion, glucose tolerance and insulin sensitivity on the one hand and the renin-angiotensin-aldosterone system on the other.

EFFECTS ON INSULIN

Insulin is a potent stimulus for hypokalaemia, sparing body potassium from urinary excretion by transporting it into cells. Potassium also appears to play a key role in the antinatriuretic effect of insulin. Insulin-induced hypokalaemia increases plasma renin and angiotensin II levels while decreasing the serum aldosterone concentration. In turn, the renin-angiotensin-aldosterone system affects glucose tolerance by modulating plasma potassium levels, which act as a stimulus for glucose-induced insulin release.

EFFECTS OF ANGIOTENSIN CONVERTING ENZYME (ACE) INHIBITION: Interference with the renin-angiotensin-aldosterone system by ACE inhibition blunts the hypokalaemic response to insulin, thereby improving glucose-induced insulin release and oral glucose tolerance. ACE inhibition, however, does not cause major changes in insulin sensitivity.

POTASSIUM AND BLOOD PRESSURE

Plasma potassium levels are inversely related to blood pressure, both in population surveys and in intervention studies. In addition, in patients with essential hypertension, the level of plasma potassium appears to predict the blood pressure response to ACE inhibition.

SUMMARY

Potassium metabolism is an important link between carbohydrate metabolism and the renin-angiotensin-aldosterone system by way of a double-feedback mechanism. Through the potential effects on blood pressure control, plasma levels of potassium represent a link between insulin and blood pressure in humans.

摘要

目的

一方面关注胰岛素分泌、糖耐量和胰岛素敏感性之间的相互作用,另一方面关注肾素 - 血管紧张素 - 醛固酮系统。

对胰岛素的影响

胰岛素是低钾血症的有力刺激因素,通过将钾转运到细胞内,使体内钾免于经尿液排泄。钾似乎在胰岛素的抗利尿钠作用中也起关键作用。胰岛素诱导的低钾血症会增加血浆肾素和血管紧张素II水平,同时降低血清醛固酮浓度。反过来,肾素 - 血管紧张素 - 醛固酮系统通过调节血浆钾水平影响糖耐量,而血浆钾水平是葡萄糖诱导胰岛素释放的刺激因素。

血管紧张素转换酶(ACE)抑制的作用:通过ACE抑制干扰肾素 - 血管紧张素 - 醛固酮系统会减弱对胰岛素的低钾血症反应,从而改善葡萄糖诱导的胰岛素释放和口服糖耐量。然而,ACE抑制不会引起胰岛素敏感性的重大变化。

钾与血压

在人群调查和干预研究中,血浆钾水平均与血压呈负相关。此外,在原发性高血压患者中,血浆钾水平似乎可预测对ACE抑制的血压反应。

总结

钾代谢通过双反馈机制是碳水化合物代谢与肾素 - 血管紧张素 - 醛固酮系统之间的重要联系。通过对血压控制的潜在影响,血浆钾水平代表了人类胰岛素与血压之间的联系。

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