Insights into the mode of action of antianginal and vasodilating agents

Angina pectoris is a clinical condition that develops from coronary atherosclerotic heart disease. The therapeutic goal to treat angina is primarily based on enhancing myocardial oxygen supply, reducing myocardial oxygen demand, or both. Nitrates, β-adrenoreceptor antagonists, and calcium entry blockers are the mainstay in the treatment of angina pectoris. Organic nitrates act as a vasodilating agent, for example, nitroglycerin, isosorbide dinitrate, and pentaerythritol tetranitrate, cause relaxation of smooth muscle, which improves oxygen supply to the myocardium. The substances that suppress the adrenergic systems of the heart such as β-adrenoblockers and Ca2+ channel blockers are also used for this purpose. β-Adrenoblockers such as propranolol, atenolol, and metoprolol reduce myocardial oxygen consumption and resting heart rate, which reduce anginal attack. Ca2+ channel blockers such as diltiazem and verapamil cause slowing down of the heart rate, strong depression of conduction at the AV node, and inhibition of contractility. Newly approved drugs include ranolazine, nicorandil, and ivabradine. Nicorandil causes vasodilation via relaxation of smooth muscle cells; ivabradine reduces heart rate by selective action on SA node; ranolazine slows down the entry of late sodium current into the myocytes and ameliorates the diastolic ventricular function and the microcirculation of the myocardium.