Mechanism of Action

The myocardial response to exercise includes an increase in heart rate and myocardial contractility. These effects are mediated in part by the sympathetic nervous system. Propranolol and other p-adrenoceptor blockers antagonize the actions of catecholamines on the heart and thereby attenuate the myocardial response to stress or exercise (Fig. 17.3). The resting heart rate is reduced by propranolol, but not to the same extent as is the decrease in exercise-induced tachycardia. Overall, propra-nolol reduces myocardial oxygen consumption for a given degree of physical activity.

Arterial blood pressure (afterload) is also reduced by propranolol. Although the mechanisms responsible for this antihypertensive effect are not completely understood, they are thought to involve (1) a reduction in cardiac output, (2) a decrease in plasma renin activity, (3) an action in the central nervous system, and (4) a resetting of the baroreceptors . Thus, propranolol may exert a part of its beneficial effects in secondary angina by decreasing three of the major determinants of myo-cardial oxygen demand, that is, heart rate, contractility, and systolic wall tension.

Propranolol and other p-blockers also have been shown to produce an increase in oxygen supply to the subendocardium of ischemic areas. The mechanism responsible for this effect is most likely related to the

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