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Positive inotropic stimulation

2002; Lippincott Williams & Wilkins; Volume: 8; Issue: 5 Linguagem: Inglês

10.1097/00075198-200210000-00005

1531-7072

Marc Léone, Jacques Alban se, Claude Martin,

Cardiac electrophysiology and arrhythmias

Adrenergic receptors transduce signals through the G proteins to regulate cardiac function. The catecholamines, via α- and β-adrenergic receptor (β-AR) stimulation, may play a role in the development of heart failure. Norepinephrine and isoproterenol can induce cardiac myocyte apoptosis. In vitro studies suggest that α-, β1-, and β2-adrenergic pathways differentially regulate cardiac myocyte apoptosis. The stimulation of β1-AR leads to cyclic AMP–dependent apoptosis, whereas that of the β2-AR elicits concurrent apoptosis and survival signals in cardiac myocytes coupled to Gs protein. Overexpression of α1-adrenergic receptors does not induce apoptosis in wild-type mice. In contrast, the heart failure observed in some murine models has to be related to an enhanced β-AR kinase expression. These recent advances make it possible to understand the beneficial effects of β-blockers in the treatment of chronic heart failure and provide novel therapeutic modalities through the stimulation of β2-ARs or the inhibition of β-AR kinase expression.