labetalol brands

Molecular formula: C19H24N2O3

Labetalol non-selectively antagonizes beta-adrenergic receptors, and selectively antagonizes alpha-1-adrenergic receptors. Following oral administration, labetalol has 3 times the beta-blocking ability than alpha-blocking ability. This increases to 6.9 times following intravenous administration. Antagonism of alpha-1-adrenergic receptors leads to vasodilation and decreased vascular resistance. This leads to a decrease in blood pressure that is most pronounced while standing. Antagonism of beta-1-adrenergic receptors leads to a slight decrease in heart rate. Antagonism of beta-2-adrenergic receptors leads to some of the side effects of labetalol such as bronchospasms, however this may be slightly attenuated by alpha-1-adrenergic antagonism. Labetalol leads to sustained vasodilation over the long term without a significant decrease in cardiac output or stroke volume, and a minimal decrease in heart rate. A specific competitive antagonist at both alpha- and beta-adrenergic receptor sites. Class II antiarrhythmic, beta-adrenoceptor-blocking agents are membrane depressant drugs that decrease the influx of sodium and calcium ions by reducing membrane bound adenylate cyclase and cAMP. The reduction in cation transport lengthens depolarization by decreasing the amplitude and slope of the transmembrane potential. Beta-adrenoceptor-blocking agents also reduce myocardial contractility by decreasing calcium release from the sarcoplasmic reticulum (the influx of calcium couples excitation and contraction by initiating the release of calcium from the sarcoplasmic reticulum). Membrane-stabilizing activity enhances the reduction in myocardial contractility in overdose with these drugs in addition to producing a quinidinelike effect of ORS widening. A direct myocardial effect also leads to myocardial depression independent of beta-adrenergic blockade and membrane stabilization. ... beta-Blockers are classified as cardioselective based on their ability to antagonize the cardiac (beta1) but not the peripheral (beta2) receptors. However, cardioselectivity is incomplete and dose dependent and disappears at high doses. /Class II beta-Blockers/ The principal physiologic action of labetalol is to competitively block adrenergic stimulation of beta-receptors within the myocardium (beta1-receptors) and within bronchial and vascular smooth muscle (beta2-receptors) and alpha1-receptors within vascular smooth muscle. In addition to inhibiting access of endogenous or exogenous catecholamines to beta-adrenergic receptors, labetalol has been shown to exhibit some intrinsic beta2-agonist activity in animals; however, the drug exerts little, if any, intrinsic beta1-agonist activity. Labetalol does not exhibit intrinsic alpha-adrenergic agonist activity. There is some evidence from animal studies suggesting that the drug may have a vasodilating effect, possibly resulting from a direct or beta2-agonist action. In animals, at doses greater than those required for alpha- or beta-adrenergic blockade, labetalol also has a membrane stabilizing effect on the heart which is similar to that of quinidine; however, this effect is unlikely to be clinically important since it occurs only at doses higher than those required for alpha- or beta-adrenergic blockade. The hemodynamic effects of labetalol are variable following oral or iv administration. Labetalol, unlike pure beta-adrenergic blocking agents, produces a dose dependent (at usual doses) decrease in systemic arterial blood pressure and systemic vascular resistance without a substantial reduction in resting heart rate, cardiac output, or stroke volume, apparently because of its combined alpha- and beta-adrenergic blocking activity. Labetalol effectively reduces blood pressure in the standing or supine position, but because of the drug's alpha1-adrenergic blocking activity, the effect on blood pressure is position dependent; labetalol induced decreases in blood pressure are greater in the standing than in the supine pos

Source: PubChem (NCBI) · compound 3869