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

Moens, An L.; Yang, Ronghua; Watts, Vabren L.; Barouch, Lili A.

doi:10.1016/j.yjmcc.2010.02.011

« Previous Next »Journal of Molecular and Cellular Cardiology
Volume 48, Issue 6 , Pages 1088-1095, June 2010

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

An L. Moens
- Johns Hopkins University School of Medicine, Div. of Cardiology, Baltimore, MD, USA
- Cardiovascular Research Institute Maastricht, University of Maastricht, Maastricht, The Netherlands
- These authors contributed equally to this work.
Ronghua Yang
- Johns Hopkins University School of Medicine, Div. of Cardiology, Baltimore, MD, USA
- These authors contributed equally to this work.
Vabren L. Watts
- Johns Hopkins University School of Medicine, Div. of Cardiology, Baltimore, MD, USA
Lili A. Barouch
- Johns Hopkins University School of Medicine, Div. of Cardiology, Baltimore, MD, USA
- Corresponding author. Johns Hopkins Medical Institutions, Div. of Cardiology, Ross Research Building 1050, 720 Rutland Ave, Baltimore, MD, 21205, USA. Tel.: +1 410 502 0188; fax: +1 410 614 0384.

Received 20 July 2009; received in revised form 8 December 2009; accepted 12 February 2010. published online 24 February 2010.

Abstract

The presence of a third β-adrenergic receptor (β3-AR) in the cardiovascular system has challenged the classical paradigm of sympathetic regulation by β1- and β2-adrenergic receptors. While β3-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 β1- and β2-AR activity. The anti-adrenergic effects induced by β3-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 β3-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.

Keywords: Beta 3 adrenergic receptor, Nitric oxide synthase, Cardiovascular, Heart failure