GPER/GPR30 and Regulation of Vascular Tone and Blood Pressure.
- Meyer MR Molecular Internal Medicine, University of Zurich, Zurich, Switzerland ; Department of Cell Biology and Physiology, University of New Mexico Health Sciences Center, Albuquerque, NM, United States.
- Prossnitz ER Department of Cell Biology and Physiology, University of New Mexico Health Sciences Center, Albuquerque, NM, United States.
- Barton M Molecular Internal Medicine, University of Zurich, Zurich, Switzerland.
- 2014-07-08
Published in:
- Immunology, endocrine & metabolic agents in medicinal chemistry. - 2011
English
Natural estrogens such as 17β-estradiol are endogenous vasodilators and have been implicated in the gender differences of hypertension. These hormones activate estrogen receptors ERα and ERβ, which mediate part of estrogen-dependent vasodilation. In addition, a novel G protein-coupled estrogen-binding receptor termed GPER/GPR30 has been identified that is expressed in the cardiovascular system. Using knock-out animals or drugs selectively targeting GPER/GPR30, a significant role for this receptor as a mediator of acute estrogen-dependent vasodilation involving nitric oxide (NO) and blood pressure-lowering activity has been demonstrated. The accumulating evidence that GPER/GPR30 is responsible for control of vascular tone indicates that this receptor may represent a novel drug target for pharmacologic treatment of hypertension in postmenopausal women and possibly also men.
- Language
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- English
- Open access status
- green
- Identifiers
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- DOI 10.2174/1871522211108040255
- PMID 24999376
- Persistent URL
- https://sonar.ch/global/documents/22182
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