Beta 3-adrenoreceptor regulation of nitric oxide in the cardiovascular system.

Autor: Moens AL; Johns Hopkins University School of Medicine, Division of Cardiology, Baltimore, MD 21205, USA., Yang R, Watts VL, Barouch LA
Jazyk: angličtina
Zdroj: Journal of molecular and cellular cardiology [J Mol Cell Cardiol] 2010 Jun; Vol. 48 (6), pp. 1088-95. Date of Electronic Publication: 2010 Feb 23.
DOI: 10.1016/j.yjmcc.2010.02.011
Abstrakt: The presence of a third beta-adrenergic receptor (beta 3-AR) in the cardiovascular system has challenged the classical paradigm of sympathetic regulation by beta1- and beta2-adrenergic receptors. While beta 3-AR's role in the cardiovascular system remains controversial, increasing evidence suggests that it serves as a "brake" in sympathetic overstimulation - it is activated at high catecholamine concentrations, producing a negative inotropic effect that antagonizes beta1- and beta2-AR activity. The anti-adrenergic effects induced by beta 3-AR were initially linked to nitric oxide (NO) release via endothelial NO synthase (eNOS), although more recently it has been shown under some conditions to increase NO production in the cardiovascular system via the other two NOS isoforms, namely inducible NOS (iNOS) and neuronal NOS (nNOS). We summarize recent findings regarding beta 3-AR effects on the cardiovascular system and explore its prospective as a therapeutic target, particularly focusing on its emerging role as an important mediator of NO signaling in the pathogenesis of cardiovascular disorders.
((c) 2010 Elsevier Ltd. All rights reserved.)
Databáze: MEDLINE
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