Although capable of antagonizing a variety of responses in a number of effectors that are mediated by both p- and a-receptors, the most important actions of labetalol are on the cardiovascular system. These effects vary from individual to individual and depend on the sympathetic and parasympathetic tone at the time of drug administration.
The most common hemodynamic effect of acutely administered labetalol in humans is a decrease in peripheral vascular resistance and blood pressure without an appreciable alteration in heart rate or cardiac output.
This pattern differs from that seen following administration with either a conventional p- or a-blocker. Acute administration of a p-blocker produces a decrease in heart rate and cardiac output with little effect on blood pressure, while acute administration of an ablocker leads to a decrease in peripheral vascular resistance and a reflexively initiated increase in cardiac rate and output. Thus, the pattern of cardiovascular responses observed after labetalol administration combines the features of p- and a-blockade, that is, a decrease in peripheral vascular resistance (due to a-blockade and direct vascular effects) without an increase in cardiac rate and output (due to p-blockade).
Prolonged oral therapy with labetalol results in cardiovascular responses similar to those obtained following conventional p-blocker administration, that is, decreases in peripheral vascular resistance, blood pressure, and heart rate. Generally, however, the decrease in heart rate is less pronounced than after administration of propranolol or other p-blockers.
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