Regulation of Sodium Transport in the Proximal Tubule by Endothelin

被引：0
|
作者：
Zhang, Ye [1 ,2 ]
Jose, Pedro A. [3 ,4 ]
Zeng, Chunyu [1 ,2 ]
机构：
[1] Third Mil Med Univ, Daping Hosp, Dept Cardiol, Chongqing 400042, Peoples R China
[2] Chongqing Inst Cardiol, Chongqing, Peoples R China
[3] George Washington Univ, Childrens Natl Med Ctr, Ctr Mol Physiol Res, Sch Med & Publ Hlth, Washington, DC USA
[4] George Washington Univ, Sch Med & Publ Hlth, Dept Pediat, Washington, DC USA
来源：
ENDOTHELIN IN RENAL PHYSIOLOGY AND DISEASE | 2011年 / 172卷
关键词：
SPONTANEOUSLY HYPERTENSIVE-RATS; NA+-K+-ATPASE; ETB-RECEPTOR; B-RECEPTORS; PLASMA ENDOTHELIN; BLOOD-PRESSURE; NITRIC-OXIDE; CONVERTING ENZYME; ANESTHETIZED RATS; EPITHELIAL-CELLS;
D O I：
暂无
中图分类号：
R5 [内科学]; R69 [泌尿科学（泌尿生殖系疾病）];
学科分类号：
1002 ; 100201 ;
摘要：
Human essential hypertension and rodent genetic hypertension are associated with increased sodium transport in the renal proximal tubule and medullary thick ascending limb of Henle. The proximal tubule, which secretes endothelin (ET), expresses the ETB receptor. Low (nM) concentrations of ET, via the ETB receptor, inhibit sodium and water transport and ATP-driven drug secretion in the proximal tubule. In contrast, very low (pM) and high nM concentrations of ET increase renal proximal sodium transport, but the receptor involved remains to be determined. The natriuretic effect of ETB receptor stimulation is impaired in spontaneously hypertensive rats, due in part to a defective interaction with D-3 dopamine and angiotensin II type 1 receptors. Impaired ETB receptor function in the renal proximal tubule may be important in the pathogenesis of genetic hypertension. Copyright (C) 2011 S. Karger AG, Basel
引用
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页码：63 / 75
页数：13
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