carvedilol brands

Molecular formula: C24H26N2O4

Carvedilol inhibits exercise induced tachycardia through its inhibition of beta adrenoceptors. Carvedilol's action on alpha-1 adrenergic receptors relaxes smooth muscle in vasculature, leading to reduced peripheral vascular resistance and an overall reduction in blood pressure. At higher doses, calcium channel blocking and antioxidant activity can also be seen. The antioxidant activity of carvedilol prevents oxidation of low density lipoprotein and its uptake into coronary circulation. Carvedilol is a nonselective beta-adrenergic blocking agent with selective alpha1-adrenergic blocking activity. The principal physiologic action of carvedilol is to competitively block adrenergic stimulation of beta-receptors within the myocardium (beta1-receptors) and within bronchial and vascular smooth muscle (beta2-receptors), and to a lesser extent alpha1-receptors within vascular smooth muscle. The beta1-antagonist activity of carvedilol is similar to that of propranolol and greater than that of labetalol, and the duration of carvedilol's effect is longer than those of labetalol and propranolol. Studies in animals indicate that the drug may exert an antioxidant effect on the myocardium and an antiproliferative effect on intimal tissue. The commercially available drug is a racemic mixture of the 2 enantiomers, (R)[+] and (S)[-], and both enantiomers have equal alpha1-adrenergic blocking activity; however, only the S(-)-enantiomer of carvedilol has beta-adrenergic blocking activity. Carvedilol does not exhibit intrinsic sympathomimetic (beta1-agonist) activity and possesses only weak membrane-stabilizing (local anesthetic) activity. Vasodilation resulting in reduced total peripheral resistance mediated through carvedilol's alpha1-adrenergic blockade and reduced sympathetic tone appear to play a major role in the drug's hypotensive effect. Carvedilol causes reductions in cardiac output, exercise-induced tachycardia, isoproterenol-induced tachycardia, and reflex orthostatic tachycardia. Clinically important beta-adrenergic blocking activity of carvedilol usually is evident within 1 hour of oral administration, and the drug's hypotensive effect is similar to that of metoprolol. Carvedilol's alpha1-adrenergic blocking effects, which contribute to the drug's hypotensive effects, generally are evident within 30 minutes of oral administration and include reductions in phenylephrine-induced pressor effects, vasodilation, and decreased peripheral vascular resistance. The dose-dependent hypotensive effect of carvedilol results in blood pressure (systolic and diastolic) reductions of 5-46% with little, if any, reflex tachycardia. This hypotensive effect occurs approximately 30 minutes after oral administration and has a maximum effect 1.5-7 hours after oral administration. The precise mechanism of the beneficial effects of carvedilol in the treatment of congestive heart failure has not been fully elucidated. beta1-Adrenergic blockade and vasodilation generally are associated with reflex tachycardia and peripheral vasoconstriction in therapeutic agents in which one of these pharmacologic effects predominates, but the combined effects of carvedilol appear to attenuate these two major untoward responses by balancing the potential adverse effects associated with adrenergic blockade and vasodilation. The drug's vasodilatory action appears to enable the patient to tolerate the negative inotropic effect of carvedilol during the initiation and titration of therapy in the treatment of compensated heart failure. For more Mechanism of Action (Complete) data for CARVEDILOL (18 total), please visit the HSDB record page.

Source: PubChem (NCBI) · compound 2585