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

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

doi:10.1016/j.yjmcc.2010.02.011

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

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

School of Medicine

Research output: Contribution to journal › Review article › peer-review

43 Scopus citations

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.

Original language	English (US)
Pages (from-to)	1088-1095
Number of pages	8
Journal	Journal of Molecular and Cellular Cardiology
Volume	48
Issue number	6
DOIs	https://doi.org/10.1016/j.yjmcc.2010.02.011
State	Published - Jun 2010

Keywords

Beta 3 adrenergic receptor
Cardiovascular
Heart failure
Nitric oxide synthase

ASJC Scopus subject areas

Molecular Biology
Cardiology and Cardiovascular Medicine

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10.1016/j.yjmcc.2010.02.011

Cite this

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title = "Beta 3-adrenoreceptor regulation of nitric oxide in the cardiovascular system",

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, Cardiovascular, Heart failure, Nitric oxide synthase",

author = "Moens, {An L.} and Ronghua Yang and Watts, {Vabren L.} and Barouch, {Lili A.}",

note = "Funding Information: This work was supported by the National Institutes of Health [ K08-HL076220 to L.A.B.]; the W.W. Smith Charitable Trust [to L.A.B.]; the American Heart Association Beginning Grant-In-Aid [ to L.A.B.]; the Belgian-American Education Foundation [to A.M.]; the Mid-Atlantic American Heart Association Postdoctoral Fellowship [to A.M.], and the Tenure Track Grant from the University of Maastricht [to A.M.]. ",

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AU - Moens, An L.

AU - Yang, Ronghua

AU - Watts, Vabren L.

AU - Barouch, Lili A.

N1 - Funding Information: This work was supported by the National Institutes of Health [ K08-HL076220 to L.A.B.]; the W.W. Smith Charitable Trust [to L.A.B.]; the American Heart Association Beginning Grant-In-Aid [ to L.A.B.]; the Belgian-American Education Foundation [to A.M.]; the Mid-Atlantic American Heart Association Postdoctoral Fellowship [to A.M.], and the Tenure Track Grant from the University of Maastricht [to A.M.].

PY - 2010/6

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N2 - 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.

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

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