Suzuki S, Kurosawa H, Koike K, Ono S, Tanita T, Fujimura S
Department of Thoracic Surgery, Tohoku University, Sendai, Japan.
Nihon Kyobu Shikkan Gakkai Zasshi. 1996 Dec;34(12):1311-6.
To test the long-term effect of a beta-adrenergic agonist on Na+/K(+)-ATPase activity in rat lung explants, we measured the activity in lung explants kept continuously in the presence or absence of 0.1 mM terbutaline for 5 days. Once it was clear that this agent increased Na+/K(+)-ATPase activity, we then performed a similar measurement in cultured alveolar type II cells from rats. Continuous exposure to 0.1 mM terbutaline enhanced the enzyme activity in those cells, and this enhancement was completely blocked by 0.01 mM of the beta-antagonist propranolol. Western blotting showed that this increase in Na+/ K(+)-ATPase activity in the cells could involve modulation of protein expression. We conclude that beta-adrenergic agonists can increase Na+/K(+)-ATPase activity in alveolar type II cell in lung explants by modulating expression of the enzyme in a long period of time.
为了测试β-肾上腺素能激动剂对大鼠肺外植体中Na+/K(+)-ATP酶活性的长期影响,我们测量了在存在或不存在0.1 mM特布他林的情况下连续培养5天的肺外植体中的该酶活性。一旦明确该药物可增加Na+/K(+)-ATP酶活性,我们随后在大鼠的培养肺泡II型细胞中进行了类似测量。持续暴露于0.1 mM特布他林可增强这些细胞中的酶活性,并且这种增强被0.01 mM的β-拮抗剂普萘洛尔完全阻断。蛋白质印迹法显示,细胞中Na+/K(+)-ATP酶活性的这种增加可能涉及蛋白质表达的调节。我们得出结论,β-肾上腺素能激动剂可通过长时间调节该酶的表达来增加肺外植体中肺泡II型细胞的Na+/K(+)-ATP酶活性。