Role of autonomic nervous system in the pathogenesis of angina pectoris

The attacks of vasospastic angina or coronary spasm can be induced by injection of epinephrine, cold pressor test, Valsalva maneuver, and exercise. The attacks induced by these procedures can be suppressed by injection of phentolamine, an alpha adrenergic blocking agent in 80 per cent of the patients. On the other hand, propranolol, a beta adrenergic blocking agent, is not only ineffective in suppressing the attacks but aggravates the attacks in 50 per cent of the patients. Thus, alpha adrenergic receptors seem to play an important role in the production of vasospastic angina. The attacks of vasospastic angina can also be induced by injection of methacholine, a parasympathomimetic agent, and this reaction is suppressed by atropine, a parasympathetic blocking agent. Thus, parasympathetic nervous system also seems to play a role in the production of vasospastic angina. The attacks of vasospastic angina can be easily induced by adrenergic or parasympathetic stimuli from midnight to early morning but is usually not provoked by these stimuli in the daytime. Thus, there is circadian variation in the reactivity of coronary arteries to adrenergic or parasympathetic stimuli. There are also weekly, monthly and yearly variations of the reactivity of coronary arteries to these stimuli. Thus, alpha adrenergic or parasympathetic activity is not the sole factor in the production of vasospastic angina. Angina pectoris caused by increased myocardial oxygen demand is induced by infusion of isoproterenol, a beta adrenergic stimulant, and is suppressed by propranolol but not by phentolamine. So, beta adrenergic receptors play an important role in the production of angina pectoris caused by increased myocardial oxygen demand or organic angina pectoris.