Positive inotropic stimulation.
Adrenergic receptors transduce signals through the G proteins to regulate cardiac function. The catecholamines, via alpha- and beta-adrenergic receptor (beta-AR) stimulation, may play a role in the development of heart failure. Norepinephrine and isoproterenol can induce cardiac myocyte apoptosis. Studies suggest that alpha-, beta1-, and beta2-adrenergic pathways differentially regulate cardiac myocyte apoptosis. The stimulation of beta1-AR leads to cyclic AMP-dependent apoptosis, whereas that of the beta2-AR elicits concurrent apoptosis and survival signals in cardiac myocytes coupled to Gs protein. Overexpression of alpha1-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 beta-AR kinase expression. These recent advances make it possible to understand the beneficial effects of beta-blockers in the treatment of chronic heart failure and provide novel therapeutic modalities through the stimulation of beta2-ARs or the inhibition of beta-AR kinase expression.
D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use; D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D017868:Cyclic AMP-Dependent Protein Kinases / Q000037:antagonists & inhibitors; D006801:Humans; D007545:Isoproterenol / Q000627:therapeutic use; D051379:Mice; D008822:Mice, Transgenic; D032383:Myocytes, Cardiac / Q000187:drug effects* / Q000378:metabolism; D011943:Receptors, Adrenergic, beta / Q000187:drug effects* / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects*; D051552:beta-Adrenergic Receptor Kinases
D000319:Adrenergic beta-Antagonists; D011943:Receptors, Adrenergic, beta; D017868:Cyclic AMP-Dependent Protein Kinases; D051552:beta-Adrenergic Receptor Kinases; D007545:Isoproterenol