NDLI: Nitric oxide and coronary vascular endothelium adaptations in hypertension

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Effect of angiotensin receptor blockade on endothelial function: focus on olmesartan medoxomil

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Nitric oxide and coronary vascular endothelium adaptations in hypertension

Content Provider	PubMed Central
Author	Levy, Andrew S. Chung, Justin Cs Kroetsch, Jeffrey T. Rush, James We
Abstract	This review highlights a number of nitric oxide (NO)-related mechanisms that contribute to coronary vascular function and that are likely affected by hypertension and thus become important clinically as potential considerations in prevention, diagnosis, and treatment of coronary complications of hypertension. Coronary vascular resistance is elevated in hypertension in part due to impaired endothelium-dependent function of coronary arteries. Several lines of evidence suggest that other NO synthase isoforms and dilators other than NO may compensate for impairments in endothelial NO synthase (eNOS) to protect coronary artery function, and that NO-dependent function of coronary blood vessels depends on the position of the vessel in the vascular tree. Adaptations in NOS isoforms in the coronary circulation to hypertension are not well described so the compensatory relationship between these and eNOS in hypertensive vessels is not clear. It is important to understand potential functional consequences of these adaptations as they will impact the efficacy of treatments designed to control hypertension and coronary vascular disease. Polymorphisms of the eNOS gene result in significant associations with incidence of hypertension, although mechanistic details linking the polymorphisms with alterations in coronary vasomotor responses and adaptations to hypertension are not established. This understanding should be developed in order to better predict those individuals at the highest risk for coronary vascular complications of hypertension. Greater endothelium-dependent dilation observed in female coronary arteries is likely related to endothelial Ca2+ control and eNOS expression and activity. In hypertension models, the coronary vasculature has not been studied extensively to establish mechanisms for sex differences in NO-dependent function. Genomic and nongenomic effects of estrogen on eNOS and direct and indirect antioxidant activities of estrogen are discussed as potential mechanisms of interest in coronary circulation that could have implications for sex- and estrogen status-dependent therapy for hypertension and coronary dysfunction. The current review identifies some important basic knowledge gaps and speculates on the potential clinical relevance of hypertension adaptations in factors regulating coronary NO function.
Ending Page	1087
Starting Page	1075
File Format	PDF
ISSN	11782048
e-ISSN	11782048
Journal	Vascular Health and Risk Management
Volume Number	5
Language	English
Publisher	Dove Medical Press
Publisher Date	2009-01-01
Access Restriction	Open
Rights Holder	Dove Medical Press
Subject Keyword	Research in Higher Education
Content Type	Text
Resource Type	Article

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