Endothelial Function in Hypertension: Victim or Culprit?

Caroline Bleakley, Paul Kevin Hamilton, Richard Pumb, Mark Harbinson, Gary Eugene McVeigh

Research output: Contribution to journalArticle

34 Citations (Scopus)

Abstract

Far from simply lining the inner surface of blood vessels, the cellular monolayer that comprises the endothelium is a highly active organ that regulates vascular tone. In health, the endothelium maintains the balance between opposing dilator and constrictor influences, while in disease, it is the common ground on which cardiovascular risk factors act to initiate the atherosclerotic process. As such, it is the site at which cardiovascular disease begins and consequently acts as a barometer of an individual's likely future cardiovascular health. The vascular endothelium is a very active organ responsible for the regulation of vascular tone through the effects of locally synthesized mediators, predominantly nitric oxide (NO), endothelial NO synthase (eNOS), and superoxide. NO is abundantly evident in normally functioning vasculature where it acts as a vasodilator, inhibits inflammation, and has an antiaggregant effect on platelets. Its depletion is both a sign and cause of endothelial dysfunction resulting from reduced activity of eNOS and amplified production of nicotinamide adenine dinucleotide oxidase, which, in turn, results in raised levels of reactive oxygen species. This cascade is the basis for reduced vascular compliance through an imbalanced regulation of tone with a predominance of vasoconstrictive elements. Further, structural changes in the microvasculature are a critical early step in the loss of normal function. This microvascular dysfunction is known to be highly predictive of future macrovascular events and is consequently a very attractive target for intervention in the hypertensive population in order to prevent cardiovascular events.

Original languageEnglish
Pages (from-to)651-4
Number of pages4
JournalJournal of clinical hypertension (Greenwich, Conn.)
Volume17
Issue number8
Early online date10 Apr 2015
DOIs
Publication statusPublished - Aug 2015

Bibliographical note

© 2015 Wiley Periodicals, Inc.

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