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W. KUPPER Coronary artery vasoconstriction is not only the mechanism responsible for Prinzmetal’s variant angina, but may also be involved in stable angina pectoris and myocardial infarction. However, the underlying patho-physiological mecha- nisms and the importance of coronary vasoconstriction in these syndromes is still largely unknown. Several hypotheses have been proposed. Sympathetic nervous activity plays a key role in the regulation of coronary blood flow, but mechanical or humoral constrictive factors may be active as well. a-adrenergic tone Adrenergic nerve fibers accompany coronary vessels of any size. The stimulation of cardiac sympathetic nerves causes an increase in coronary blood flow. If, however, chronotropic and inotropic effects of adrenergic stimulation are sup- pressed pharmacologically by beta-adrenoceptor blockade, a reduction in flow is observed. Thus, the primary effect of sympathetic stimulation on the coronary arteries is the alpha-adrenergic mediated vasoconstriction. Functionally inner- vated alpha-adrenoceptors have been documented both in large coronary con- ductance arteries and in the small resistance vessels. Animal studies and a human study have documented that a permanent constrictor tone is present on the coronary circulation both at rest and during exercise; this condition could be prevented with alpha-adrenoceptor blockade or was absent after heart transplan- tation. Therefore, alpha-adrenoceptor mediated coronary constriction is an at- tractive hypothesis as a possible pathophysiological mechanism of inappropriate coronary vasoconstriction and cororiary vasospasm.
