化学
医学
重吸收
上皮钠通道
肾素-血管紧张素系统
肾
协同运输机
平衡
远曲小管
作者
Soline Bourgeois,Carsten A. Wagner
出处
期刊:Current Opinion in Nephrology and Hypertension
[Ovid Technologies (Wolters Kluwer)]
日期:2021-01-01
卷期号:30 (1): 131-137
被引量:1
标识
DOI:10.1097/mnh.0000000000000669
摘要
PURPOSE OF REVIEW
Pendrin resides on the luminal membrane of type B intercalated cells in the renal collecting tubule system mediating the absorption of chloride in exchange for bicarbonate. In mice or humans lacking pendrin, blood pressure is lower, and pendrin knockout mice are resistant to aldosterone-induced hypertension. Here we discuss recent findings on the regulation of pendrin.
RECENT FINDINGS
Pendrin activity is stimulated during alkalosis partly mediated by secretin. Also, angiotensin II and aldosterone stimulate pendrin activity requiring the mineralocorticoid receptor in intercalated cells. Angiotensin II induces dephosphorylation of the mineralocorticoid receptor rendering the receptor susceptible for aldosterone binding. In the absence of the mineralocorticoid receptor in intercalated cells, angiotensin II does not stimulate pendrin. The effect of aldosterone on pendrin expression is in part mediated by the development of hypokalemic alkalosis and blunted by K-supplements or amiloride. Part of the blood pressure-increasing effect of pendrin is also mediated by its stimulatory effect on the epithelial Na-channel in neighbouring principal cells.
SUMMARY
These findings identify pendrin as a critical regulator of renal salt handling and blood pressure along with acid--base balance. A regulatory network of hormones fine-tuning activity is emerging. Drugs blocking pendrin are being developed.
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