Hori M, Nakatsubo N, Kagiya T, Iwai K, Sato H, Iwakura K, Kitabatake A, Kamada T
First Department of Medicine, Osaka University Medical School, Japan.
Jpn Circ J. 1990 May;54(5):535-9. doi: 10.1253/jcj.54.535.
It is reported that Na+ influx contributes to stretch-induced cardiac hypertrophy. Na+ influx may also be involved in cardiac hypertrophy induced by catecholamine. In the present study, to test whether Na+/H+ exchange plays an important role in norepinephrine-induced cardiac hypertrophy, the effect of Na+/H+ exchange inhibitor, amiloride on protein synthesis was studied in cultured neonatal rat cardiomyocytes in serum free medium. [3H]Phenylalanine uptake was determined 24 and 48 hours after administration of norepinephrine with and without amiloride. In the control, norepinephrine increased [3H]phenylalanine uptake in a dose dependent manner (10(-5)-10(-7) M). Prazosin (10(-7) M) and amiloride (10(-5)-10(-4) M) significantly attenuated the norepinephrine mediated protein synthesis. These results indicate that alpha 1-adrenergic stimulation enhances the protein synthesis through activation of Na+/H+ exchange. Therefore, Na+ influx and/or PH increase may play a key role in cardiac hypertrophy.
据报道，钠离子内流有助于牵张诱导的心肌肥大。钠离子内流也可能参与儿茶酚胺诱导的心肌肥大。在本研究中，为了检测钠氢交换在去甲肾上腺素诱导的心肌肥大中是否起重要作用，在无血清培养基中培养的新生大鼠心肌细胞中研究了钠氢交换抑制剂氨氯地平对蛋白质合成的影响。在给予去甲肾上腺素并添加或不添加氨氯地平24和48小时后，测定[3H]苯丙氨酸摄取量。在对照组中，去甲肾上腺素以剂量依赖方式（10^(-5)-10^(-7)M）增加[3H]苯丙氨酸摄取量。哌唑嗪（10^(-7)M）和氨氯地平（10^(-5)-10^(-4)M）显著减弱去甲肾上腺素介导的蛋白质合成。这些结果表明，α1-肾上腺素能刺激通过激活钠氢交换增强蛋白质合成。因此，钠离子内流和/或pH升高可能在心肌肥大中起关键作用。
