Year: 2000
Type: editorial
Abstract: t is now generally accepted that chronically elevated stimulation of the cardiac -adrenergic system is toxic to the heart and that such stimulation may contribute to the pathogenesis of congestive heart failure of various causes.Administration of either -adrenergic agonists or phosphodiesterase inhibitors has been shown to decrease survival of patients with chronic heart failure, even though they produce immediate and long-term hemodynamic benefits.1 Moreover, in human heart failure, as well as in several animal models, elevated circulating catecholamines lead, via various compensatory mechanisms, to decreased levels and functional activity of cardiac  1 -adrenergic receptors ( 1 ARs) and thus to marked desensitization of the heart to inotropic -adrenergic stimulation.
Source: Circulation
Language: English
Subfield: Molecular Biology
Domain: Life Sciences
Open Access status: green
OpenAlex ID: W2149649063