Document Detail

Oxidant and redox signaling in vascular oxygen sensing mechanisms: basic concepts, current controversies, and potential importance of cytosolic NADPH.
MedLine Citation:
PMID:  16002998     Owner:  NLM     Status:  MEDLINE    
Vascular smooth muscle (VSM) derived from pulmonary arteries generally contract to hypoxia, whereas VSM from systemic arteries usually relax, indicating the presence of basic oxygen-sensing mechanisms in VSM that are adapted to the environment from which they are derived. This review considers how fundamental processes associated with the generation of reactive oxygen species (ROS) by oxidase enzymes, the metabolic control of cytosolic NADH, NADPH and glutathione redox systems, and mitochondrial function interact with signaling systems regulating vascular force in a manner that is potentially adapted to be involved in Po2 sensing. Evidence for opposing hypotheses of hypoxia, either decreasing or increasing mitochondrial ROS, is considered together with the Po2 dependence of ROS production by Nox oxidases as sensors potentially contributing to hypoxic pulmonary vasoconstriction. Processes through which ROS and NAD(P)H redox changes potentially control interactive signaling systems, including soluble guanylate cyclase, potassium channels, and intracellular calcium are discussed together with the data supporting their regulation by redox in responses to hypoxia. Evidence for hypothesized potential differences between systemic and pulmonary arteries originating from properties of mitochondrial ROS generation and the redox sensitivity of potassium channels is compared with a new hypothesis in which differences in the control of cytosolic NADPH redox by the pentose phosphate pathway results in increased NADPH and Nox oxidase-derived ROS in pulmonary arteries, whereas lower levels of glucose-6-phosphate dehydrogenase in coronary arteries may permit hypoxia to activate a vasodilator mechanism controlled by oxidation of cytosolic NADPH.
Michael S Wolin; Mansoor Ahmad; Sachin A Gupte
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.; Review    
Journal Detail:
Title:  American journal of physiology. Lung cellular and molecular physiology     Volume:  289     ISSN:  1040-0605     ISO Abbreviation:  Am. J. Physiol. Lung Cell Mol. Physiol.     Publication Date:  2005 Aug 
Date Detail:
Created Date:  2005-07-08     Completed Date:  2005-08-16     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  100901229     Medline TA:  Am J Physiol Lung Cell Mol Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  L159-73     Citation Subset:  IM    
Dept. of Physiology, Basic Science Bldg., Rm. 604, New York Medical College, Valhalla, NY 10595, USA.
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MeSH Terms
Blood Vessels / metabolism*
Cytosol / metabolism*
NADH, NADPH Oxidoreductases / metabolism
NADP / metabolism*
Oxygen / metabolism*
Reactive Oxygen Species / metabolism*
Signal Transduction*
Grant Support
Reg. No./Substance:
0/Oxidants; 0/Reactive Oxygen Species; 53-59-8/NADP; 7782-44-7/Oxygen; EC 1.6.-/NADH, NADPH Oxidoreductases

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