Studies in myopathic hamsters have described an increase in
calcium antagonist binding sites, which is presumably associated with an increase in the number of
calcium channels. Such an abnormality might predispose the heart to further myocardial damage from
calcium overload. We tested the hypothesis that
calcium antagonist binding sites are increased in human
idiopathic dilated cardiomyopathy by examining [3H]
PN 200-110 and [3H]
nitrendipine binding in membranes prepared from nonfailing controls and severely failing ventricles with
idiopathic dilated cardiomyopathy. Despite the fact that beta receptor density was decreased by 50% in failing hearts (
iodocyanopindolol Bmax 84.4 +/- 8.9 fmol/mg
protein in nonfailing hearts vs 42.9 +/- 3.2 fmol/mg in failing hearts, P less than 0.01),
dihydropyridine calcium antagonist binding sites were not reduced significantly by
heart failure. Maximum binding of [3H]
PN 200-110 was 92.9 +/- 19.4 fmol/mg
protein in membranes derived from failing ventricles, and 93.5 +/- 17.4 fmol/mg in membranes derived from nonfailing ventricles (P = NS); values for [3H]
nitrendipine maximum binding were similar to those for [3H]
PN 200-110 and also were not reduced significantly in failing ventricles. Additionally, the dissociation constants (KD) for [3H]
nitrendipine and [3H]
PN 200-110 were not significantly different in failing and nonfailing heart. We conclude that
dihydropyridine calcium antagonist binding sites are not altered significantly in the failing human left ventricle with
idiopathic dilated cardiomyopathy.