[3H]-nitrendipine binding sites in normal and cardiomyopathic hamsters: absence of a selective increase in putative calcium channels in cardiomyopathic hearts.
The number of putative calcium channels in cardiac muscle from young adult hamsters (60 days old) was compared in normal (F1B) hamsters and two different mutant strains (CHF 146 and Bio 14.6) which express cardiomyopathy and muscular dystrophy. Equilibrium binding assays of high affinity sites for [3H]-nitrendipine in ventricular homogenate preparations showed that the maximum number of [3H]-nitrendipine binding sites (Bmax), which corresponds to the number of putative calcium channels, was not significantly different in normal and cardiomyopathic hearts: 79(SEM 9), 64(14) and 69(10) fmol.mg-1 protein in 4-6 hearts from F1B, Bio 14.6 and CHF 146 hamster strains, respectively. Similar results were obtained with binding data after partial purification of the preparation. These data are in agreement with earlier studies comparing two normal strains (CHF 148 and random bred Syrian hamsters) with cardiomyopathic (CHF 146) hamsters, and conflict with other studies comparing normal and cardiomyopathic hamsters. Comparisons with the conflicting data suggest (a) that change in the number of high affinity [3H]-nitrendipine binding sites is not responsible for calcium overload and cell necrosis in cardiomyopathy, and (b) that increased numbers of low affinity [3H]-nitrendipine binding sites may emerge in cardiomyopathic hearts.
Howlett
S E
SE
Department of Pharmacology, Faculty of Medicine, University of Alberta, Edmonton, Canada.
Rafuse
V F
VF
Gordon
T
T
D000818:Animals; D001665:Binding Sites; D015220:Calcium Channels / Q000032:analysis*; D009202:Cardiomyopathies / Q000378:metabolism*; D006224:Cricetinae; D008297:Male; D008647:Mesocricetus; D009137:Muscular Dystrophy, Animal / Q000378:metabolism; D009206:Myocardium / Q000378:metabolism; D009568:Nitrendipine / Q000378:metabolism*; D011869:Radioligand Assay
D015220:Calcium Channels; D009568:Nitrendipine