The great extramural coronary stem arteries (as well as extramural collaterals and anastomoses) deserve particular interest with respect to their peculiar susceptibility to autonomic neurotransmitters and drugs. Obviously these arteries, preferentially affected by atherosclerotic processes, are most responsive to such vasodilators which block vascular tone and contractility by interference with Ca-dependent excitation-contraction coupling. This applies first of all to the new pharmacological family of Ca-antagonists but also to the classical nitrites. As we have emphasized in 1971. Ca-antagonism is a new principle of coronary vascular dilation with profound clinical implications (5). In fact, the Ca-antagonists have become, within a few years, the drugs of choice for the treatment of all spastic forms of angina. By contrast adenosine, dipyridamole, chromonar and theophylline preferably dilate the small intramural resistance vessels, but do not significantly reflex the extramural stem arteries. Therefore, in coronary heart disease, the latter drugs do usually not produce major circulatory improvement.