Nakanishi H, Makino N, Hata T, Matsui H, Yano K, Yanaga T
Department of Bioclimatology and Medicine, Kyushu University, Beppu, Japan.
Am J Physiol. 1989 Aug;257(2 Pt 2):H349-56. doi: 10.1152/ajpheart.1989.257.2.H349.
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.
为研究压力超负荷所致心肌肥厚时肌膜的钙离子转运活性，对大鼠进行主动脉缩窄术28天。与假手术组大鼠相比，主动脉缩窄组大鼠的心重/体重比增加了46%。肥厚心脏肌膜中哇巴因敏感的钠钾ATP酶活性与对照制剂无差异。与对照囊泡相比，肥厚心脏肌膜囊泡中钠依赖的钙离子摄取初始速率提高了53%。肥厚心脏肌膜中ATP依赖的钙离子摄取和钙离子刺激的腺苷三磷酸酶（ATP酶）活性增加了35%。用[5-甲基-3H]尼群地平结合法估计的肥厚心脏肌膜中钙离子通道数量减少了33%。肥厚心脏制剂中的总磷脂和各磷脂含量与对照无差异，只是磷脂酰胆碱和磷脂酰乙醇胺含量显著增加。22周龄自发性高血压大鼠肥厚心脏的肌膜制剂表现出钠钙交换和钙泵活性的变化（与主动脉缩窄心脏中观察到的相似），而钠钾ATP酶活性降低，[3H]尼群地平结合增加，磷脂含量无差异。因此，尽管两种类型的心肌肥厚存在差异，但这些结果提示肌膜钙离子转运活性发生改变，这可能是心肌肥厚发展过程中从心肌细胞中清除钙离子的一种适应性机制。
