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European Journal of Heart Failure 2007 9(12):1163-1171; doi:10.1016/j.ejheart.2007.10.006
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© 2007 European Society of Cardiology

Sepsis is associated with an upregulation of functional β3 adrenoceptors in the myocardium

S. Moniotte1, C. Belge1, B. Sekkali, P.B. Massion2, B. Rozec, C. Dessy and J.-L. Balligand*

Unit of Pharmacology and Therapeutics FATH 5349, Université catholique de Louvain Brussels — Belgium

* Corresponding author. Unit of Pharmacology and Therapeutics FATH 5349, Université catholique de Louvain 52 avenue Mounier, B1200 Brussels, Belgium. Tel.: +32 2 764 5260; fax: +32 2 764 5269. Balligand{at}mint.ucl.ac.be (J.-L. Balligand)


  Abstract

Objective: To analyze the implication of the β3-adrenoceptor (β3-AR) pathway in human septic myocardium and a murine model of sepsis, a condition associated with myocardial depression.

Methods and results: β3-AR and eNOS protein abundance were increased (332±66.4% and 218±39.3; P<0.05) in hearts from septic patients. The effect of BRL37344, a β3-AR-preferential agonist, was analyzed by videomicroscopy on the contractility of neonatal mouse ventricular myocytes (NMVM) incubated with conditioned medium from LPS-stimulated cultured macrophages (Mc-LPS+ medium). Stimulation of untreated NMVM with BRL37344 dose-dependently decreased the amplitude of contractile shortening (P<0.05). This response was abolished by L-NAME (NOS inhibitor). Incubation in Mc-LPS+ medium potentiated the depressing effect of BRL37344 (P<0.05) as well as of SR58611A (P<0.05) in wild-type myocytes. Importantly, the contractile depression was abrogated in cardiomyocytes from β3-AR KO mice.

Conclusions: β3-AR are upregulated during sepsis in the human myocardium and by cytokines in murine cardiomyocytes, where they mediate an increased negative inotropic response to β3 agonists. Activation of the β3-AR pathway by catecholamines may contribute to the myocardial dysfunction in sepsis.

Key Words: Receptors • Adrenergic • Beta • Cytokines • Pharmacology • Nitric oxide synthase • Myocardial contraction

Received March 8, 2007; Revised September 21, 2007; Accepted October 18, 2007

1 These authors equally contributed to this work.

2 Present address: Department of General Intensive Care, University Hospital Center, Sart-Tilman, B-4000 Liège, Belgium.


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