title: Defective Ca2+-pumping ATPase of heart sarcolemma from cardiomyopathic hamster.
abstract: The Syrian cardiomyopathic hamster has a hereditary disease characterized by a progressive myocyte necrosis and intracellular calcium overload. Several systems in the heart sarcolemma that regulate the rate of Ca2+ entry or efflux were examined. There is a selective decrease of Ca2+-pumping ATPase activity in the heart sarcolemma of 40-day-old myopathic hamsters, while the Na+-Ca2+ exchange system and the ouabain-sensitive (Na+ + K+)-ATPase activity remain intact. This age-dependent decrease in Ca2+-ATPase activity closely parallels the time course of lesion development. Both the affinity for Ca2+ (Km) and the maximal velocity (Vmax) of the Ca2+-dependent ATP hydrolysis are altered. In addition, there is also an increased number of calcium channel receptor binding sites. Thus the data suggest that the imbalance in Ca2+ fluxes across the cardiac plasma membrane may be involved in the pathogenesis of this cardiomyopathy.
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D000375:Aging / Q000378:metabolism; D000818:Animals; D002118:Calcium / Q000378:metabolism; D000252:Calcium-Transporting ATPases / Q000378:metabolism*; D009202:Cardiomyopathies / Q000201:enzymology* / Q000235:genetics; D002352:Carrier Proteins / Q000378:metabolism; D006224:Cricetinae; D007700:Kinetics; D008647:Mesocricetus; D009206:Myocardium / Q000201:enzymology*; D012508:Sarcolemma / Q000201:enzymology*; D019831:Sodium-Calcium Exchanger
chemical_list: D002352:Carrier Proteins; D019831:Sodium-Calcium Exchanger; D000255:Adenosine Triphosphate; D000252:Calcium-Transporting ATPases; D002118:Calcium