Endothelial nitric oxide synthase in the microcirculation
- Cell Mol Life Sci. 2015 Dec;72(23):4561-75. doi: 10.1007/s00018-015-2021-0.
- 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. [email protected].
- 7. Department of Molecular Physiology and Biophysics, University of Virginia School of Medicine, Charlottesville, USA. [email protected].
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.