Prostaglandin E2 modulation of blood pressure homeostasis: Studies in rodent models

被引:25
作者
Swan, Christina E. [3 ]
Breyer, Richard M. [1 ,2 ,3 ]
机构
[1] Vanderbilt Univ, Med Ctr, Div Nephrol & Hypertens, Dept Med, Nashville, TN 37232 USA
[2] Vet Affairs Hosp, Dept Med, Nashville, TN 37232 USA
[3] Vanderbilt Univ, Med Ctr, Dept Pharmacol, Nashville, TN 37232 USA
关键词
Prostaglandin E-2; Hypertension; GPCR; Mouse; Rat; EP receptors; Blood pressure; Kidney; MICE LACKING; PROSTANOID RECEPTORS; OXIDATIVE STRESS; ANGIOTENSIN-II; E SYNTHASE; HYPERTENSION; EP2; RATS; IDENTIFICATION; STIMULATION;
D O I
10.1016/j.prostaglandins.2011.07.001
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Hypertension is a well established risk factor for cardiovascular diseases such as stroke and is the leading cause of chronic kidney failure. Although a number of pharmacologic agents are available for the treatment of hypertension including agents that affect the renin-angiotensin-aldosterone system (RAAS), unmet needs in the treatment of hypertension suggest that identification of novel pharmacological targets would be an important healthcare goal. One potential target is prostaglandin E-2 (PGE(2)), a potent lipid mediator with a diverse and sometimes opposing range of biological effects. PGE(2) signals through four subtypes of G-protein coupled receptors designated EP1 through EP4. PGE(2) functions primarily as a vasodepressor; under certain conditions PGE(2) administration mediates vasopressor activity. This review focuses on the current understanding of the roles of PGE(2) receptors in vascular reactivity, hypertension and end-organ damage. Published by Elsevier Inc.
引用
收藏
页码:10 / 13
页数:4
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