(LVEF) into those with mild cardiac dysfunction (LVEF < 0.50 > 0.40) and severe heart failure (LVEF < 0.20) and given graded sequential infusions of dobutamine and calcium gluconate. Those with severe cardiac dysfunction had marked impairment of the dobutamine dP/dt and stroke work index response, whereas these responses to calcium did not differ in the two groups. These data indicate that in the intact human heart (1)

[3H]‐nitrendipine binding data and isolated tissue response for five calcium antagonists were evaluated in rabbit myocardium and aorta. The [3H]‐nitrendipine binding site was qualitatively identical in myocardium and aorta, as the [3H]‐nitrendipine KD, KIs for nicardipine and nifedipine and interactions with verapamil, D600‐and diltiazem were not different in aortic and cardiac membranes prepared by similar means. In contrast, the inhibition of the Ca2+‐induced contractile response in right ventricular myocardium and aortic ring segments indicated a > 10,000 fold selectivity of nicardipine for antagonism of vascular responses. This resulted in a different order of potency for calcium antagonist interaction with the [3H]‐nitrendipine binding site in cardiac membranes (nicardipine > nifedipine > D600 > verapamil > diltiazem) as compared to antagonism of myocardial tissue response (D600 > verapamil > nifedipine > nicardipine > diltiazem). In heart the difference between the potency of nicardipine in binding experiments and tissue response approached 4 orders of magnitude. We conclude that tissue response selectivity of calcium antagonists is not explained by heterogeneity of [3H]‐nitrendipine binding sites.