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Cell Mol Life Sci. 2015 Dec;72(23):4561-75. doi: 10.1007/s00018-015-2021-0. Epub 2015 Aug 25.

Endothelial nitric oxide synthase in the microcirculation.

Author information

1
College of Pharmacy, Dalian Medical University, Dalian, 116044, China.
2
Robert M. Berne Cardiovascular Research Center, University of Virginia School of Medicine, P.O. Box 801394, Charlottesville, VA, 22908, USA.
3
Department of Molecular Physiology and Biophysics, University of Virginia School of Medicine, Charlottesville, USA.
4
Department of Pharmacology, University of Virginia School of Medicine, Charlottesville, USA.
5
Department of Chemistry, University of Virginia, Charlottesville, USA.
6
Robert M. Berne Cardiovascular Research Center, University of Virginia School of Medicine, P.O. Box 801394, Charlottesville, VA, 22908, USA. brant@virginia.edu.
7
Department of Molecular Physiology and Biophysics, University of Virginia School of Medicine, Charlottesville, USA. brant@virginia.edu.

Abstract

Endothelial nitric oxide synthase (eNOS, NOS3) is responsible for producing nitric oxide (NO)--a key molecule that can directly (or indirectly) act as a vasodilator and anti-inflammatory mediator. In this review, we examine the structural effects of regulation of the eNOS enzyme, including post-translational modifications and subcellular localization. After production, NO diffuses to surrounding cells with a variety of effects. We focus on the physiological role of NO and NO-derived molecules, including microvascular effects on vessel tone and immune response. Regulation of eNOS and NO action is complicated; we address endogenous and exogenous mechanisms of NO regulation with a discussion of pharmacological agents used in clinical and laboratory settings and a proposed role for eNOS in circulating red blood cells.

KEYWORDS:

Endothelial nitric oxide synthase; Endothelium; Microcirculation; Nitric oxide

PMID:
26390975
PMCID:
PMC4628887
DOI:
10.1007/s00018-015-2021-0
[Indexed for MEDLINE]
Free PMC Article

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