Beta-adrenergic receptors in failing human myocardium.
In the human heart the beta-adrenergic receptor-G-protein-adenylyl cyclase system is the most powerful physiologic mechanism to acutely increase contractility and/or heart rate. In the failing human myocardium beta 1-adrenergic receptor number is decreased, and this is accompanied by a reduced beta 1-adrenergic receptor mediated positive inotropic effect. Cardiac beta 2-adrenergic receptor number may or may not decrease; however, beta 2- adrenergic receptor mediated positive inotropic effects are also reduced, possibly because the functional activity of myocardial Gi is increased, thereby inhibiting cyclic AMP formation. The aging human heart shows some similarities with the failing human heart: in both settings, of chronic heart failure and age, beta-adrenergic receptor mediated effects and all other cyclic AMP dependent effects are depressed and Gi-protein is increased.
Brodde
O E
OE
Institute of Pharmacology University of Halle-Wittenberg, Halle (Saale) Germany.
D000375:Aging / Q000502:physiology; D002908:Chronic Disease; D000242:Cyclic AMP / Q000378:metabolism; D018450:Disease Progression; D019204:GTP-Binding Proteins / Q000378:metabolism; D006333:Heart Failure / Q000378:metabolism* / Q000503:physiopathology; D006801:Humans; D009200:Myocardial Contraction / Q000502:physiology; D009206:Myocardium / Q000378:metabolism*; D010766:Phosphorylation; D010770:Phosphotransferases / Q000378:metabolism; D011943:Receptors, Adrenergic, beta / Q000378:metabolism*
D011943:Receptors, Adrenergic, beta; D000242:Cyclic AMP; D010770:Phosphotransferases; D019204:GTP-Binding Proteins