Dihydropyridine (DHP) calcium antagonists are established drugs in the management of hypertension and chronic stable angina. However, recently a dose-related increase in the mortality of patients with coronary artery disease with nifedipine has been suggested. The conclusions of this study were seriously contradicted. Therefore, in our laboratory, the effect of the DHP calcium antagonist nisoldipine on ischaemic myocardial blood flow and function, infarct size, and the functional recovery of reversibly injured, reperfused myocardium was once more investigated in controlled in vivo models. In anaesthetized dogs, in the presence of a severe coronary artery stenosis, intravenous nisoldipine decreased poststenotic subendocardial blood flow and contractile function when arterial pressure was decreased. In contrast, when hypotension was prevented by inflation of an intra-aortic balloon, no aggravation of myocardial ischaemia was seen. During exercise, when aortic pressure is raised by catecholamines, nisoldipine may therefore not exert a proischaemic effect, but may rather improve regional myocardial blood flow and function in the ischaemic region. As has been shown for nifedipine, the f
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