The activation of sympathetic nerves plays a significant role in the initiation of acute myocardial ischemia. In this review the effects of sympathetic nerves on coronary blood flow are summarized. Under physiological conditions the increase in myocardial performance during sympathetic activation is accompanied by metabolic coronary vasodilation. The resulting increase in coronary blood flow is limited by about 30% by alpha-adrenergic coronary constriction. Extravascular compression and beta-adrenergic coronary dilation are of minor importance during sympathetic activation. With exhausted coronary reserve distal to severe coronary stenoses metabolic vasodilation during sympathetic activation is not possible any more; an alpha 2-adrenoceptor-mediated coronary vasoconstriction now predominates. This coronary constriction induces ischemia of the post-stenotic myocardium. The alpha-antagonists Phentolamine and Rauwolscine as well as the calcium-antagonist Nifedipine prevent poststenotic coronary constriction and myocardial ischemia. Also in the genesis of coronary arterial spasm the sympathetic nervous system may play an important role; the constriction of epicardial coronary arteries is mediated by alpha 1-adrenoceptors. The sympathetic nervous system is not only involved in the initiation of myocardial ischemia, but is also activated by ischemia. This feedback-activation of sympathetic nerves leads to an aggravation of myocardial ischemia.