Adrenergic mechanisms in congestive heart failure.
The normal control of cardiovascular function exerted by the sympathetic nervous system is disturbed in congestive heart failure. The failing pump function of the heart evokes an increase in sympathetic activity which may be reflected in increased levels of plasma noradrenaline. However, these levels are generally below the concentrations needed to activate the adrenergic effector systems, indicating that the cardiovascular consequences of the increased sympathetic activity is not mediated by circulating noradrenaline. In the failing human heart there is a decrease in beta-adrenoceptor density which is related to decreasing ventricular function. This finding suggests that the myocardium is exposed to high concentrations of noradrenaline, inducing downregulation of the receptor number, despite the fact that in the failing heart the noradrenaline stores are reduced. In heart failure the plasma noradrenaline concentration was found to be directly related to mortality and was suggested to provide a better guide to prognosis than other commonly measured indexes of cardiac performance.
D000322:Adrenergic Agonists / Q000627:therapeutic use; D000818:Animals; D000242:Cyclic AMP / Q000502:physiology; D006152:Cyclic GMP / Q000502:physiology; D006333:Heart Failure / Q000188:drug therapy / Q000503:physiopathology*; D006801:Humans; D009131:Muscle, Smooth, Vascular / Q000502:physiology; D009638:Norepinephrine / Q000097:blood; D011379:Prognosis; D011941:Receptors, Adrenergic / Q000502:physiology*; D011942:Receptors, Adrenergic, alpha / Q000502:physiology; D011943:Receptors, Adrenergic, beta / Q000502:physiology; D012039:Regional Blood Flow; D000254:Sodium-Potassium-Exchanging ATPase / Q000502:physiology; D013268:Stimulation, Chemical
D000322:Adrenergic Agonists; D011941:Receptors, Adrenergic; D011942:Receptors, Adrenergic, alpha; D011943:Receptors, Adrenergic, beta; D000242:Cyclic AMP; D000254:Sodium-Potassium-Exchanging ATPase; D006152:Cyclic GMP; D009638:Norepinephrine