title: Sarcolemmal Ca2+ transport activities in cardiac hypertrophy caused by pressure overload.
abstract: To examine Ca2+ transport activities in sarcolemmal membrane in cardiac hypertrophy caused by pressure overload, rats were subjected to aortic banding for 28 days. Heart-to-body weight ratio was increased by 46% in aortic-banded animals in comparison with the sham-operated rats. Ouabain-sensitive Na+-K+-ATPase activity in sarcolemma (SL) from hypertrophied hearts was not different from that in the control preparation. The initial rate of Na+-dependent Ca2+ uptake in SL vesicles from the hypertrophied hearts was stimulated by 53% compared with the control vesicles. ATP-dependent Ca2+ uptake and Ca2+-stimulated adenosinetriphosphatase (ATPase) activities in SL from hypertrophied hearts were increased by 35%. The number of Ca2+ channels estimated by [5-methyl-3H]nitrendipine binding was decreased by 33% in SL from hypertrophied hearts. Total and individual phospholipid contents in the hypertrophied heart preparations were not different from those in the control, except that phosphatidylcholine and phosphatidylethanolamine contents were significantly increased. Sarcolemmal preparations from hypertrophied hearts from the 22-wk-old spontaneously hypertensive rats exhibited changes in Na+-Ca2+ exchange and Ca2+-pump activities (similar to those observed in banded hearts), whereas the Na+-K+-ATPase activity decreased, [3H]nitrendipine binding increased, and phospholipid contents were not different. Thus, although differences were defined between two types of hypertrophy, these results suggest alterations in the sarcolemmal Ca2+ transport activities that may serve as an adaptive mechanism for the removal of Ca2+ from the myocardial cells during the development of cardiac hypertrophy.
authors.affiliation: Department of Bioclimatology and Medicine, Kyushu University, Beppu, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Nakanishi
authors.forename: N
authors.initials: N
authors.lastname: Makino
authors.forename: T
authors.initials: T
authors.lastname: Hata
authors.forename: H
authors.initials: H
authors.lastname: Matsui
authors.forename: K
authors.initials: K
authors.lastname: Yano
authors.forename: T
authors.initials: T
authors.lastname: Yanaga
mesh_terms: D000818:Animals; D001012:Aorta, Abdominal / Q000502:physiology; D001794:Blood Pressure; D017301:Ca(2+) Mg(2+)-ATPase / Q000378:metabolism; D002118:Calcium / Q000378:metabolism*; D015220:Calcium Channels; D000252:Calcium-Transporting ATPases / Q000378:metabolism*; D006332:Cardiomegaly / Q000378:metabolism* / Q000503:physiopathology; D002352:Carrier Proteins / Q000378:metabolism; D002784:Cholesterol / Q000032:analysis; D006321:Heart / Q000503:physiopathology; D007700:Kinetics; D008297:Male; D008563:Membrane Lipids / Q000032:analysis; D009206:Myocardium / Q000378:metabolism*; D009568:Nitrendipine / Q000378:metabolism; D010743:Phospholipids / Q000032:analysis; D051381:Rats; D011918:Rats, Inbred SHR; D011919:Rats, Inbred Strains; D011921:Rats, Inbred WKY; D011978:Receptors, Nicotinic / Q000378:metabolism; D012016:Reference Values; D012508:Sarcolemma / Q000378:metabolism*; D019831:Sodium-Calcium Exchanger; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism
chemical_list: D015220:Calcium Channels; D002352:Carrier Proteins; D008563:Membrane Lipids; D010743:Phospholipids; D011978:Receptors, Nicotinic; D019831:Sodium-Calcium Exchanger; D002784:Cholesterol; D009568:Nitrendipine; D017301:Ca(2+) Mg(2+)-ATPase; D000252:Calcium-Transporting ATPases; D000254:Sodium-Potassium-Exchanging ATPase; D002118:Calcium