Dihydropyridine receptor binding sites in the cardiomyopathic hamster heart are unchanged from control.
An increase in the number of voltage dependent calcium channels has been implicated in the overload of calcium found in cardiac tissue of the cardiomyopathic hamster. We examined the binding of [3H]-(+)PN200110 to dihydropyridine receptors in cardiac muscle membranes from TO cardiomyopathic hamsters. When compared to random bred controls, there were no differences in either the Bmax or the KD for [3H]-(+)PN200110 binding using homogenates from 35 to 41-day-old TO cardiomyopathic hearts. In 8 to 9-month-old myopathic animals there were only small decreases in Bmax with no change in KD. We suggest that the calcium overload observed in cardiomyopathic hamster heart may not be due to an increased density of calcium channels as estimated by high affinity dihydropyridine receptor binding sites.
Bazan
E
E
Department of Pharmacology and Cell Biophysics, University of Cincinnati College of Medicine, OH 45267-0575.
Sole
M J
MJ
Schwartz
A
A
Johnson
C L
CL
D000818:Animals; D002121:Calcium Channel Blockers / Q000378:metabolism*; D015220:Calcium Channels / Q000378:metabolism*; D009202:Cardiomyopathies / Q000378:metabolism*; D006224:Cricetinae; D017275:Isradipine; D008297:Male; D009206:Myocardium / Q000378:metabolism*; D010069:Oxadiazoles / Q000378:metabolism*; D011978:Receptors, Nicotinic / Q000378:metabolism*
D002121:Calcium Channel Blockers; D015220:Calcium Channels; D010069:Oxadiazoles; D011978:Receptors, Nicotinic; D017275:Isradipine