Sunga P S, Rabkin S W
University Hospital Research Centre (Shaughnessy Site), University of British Columbia, Vancouver, Canada.
Hypertension. 1992 Nov;20(5):633-42. doi: 10.1161/01.hyp.20.5.633.
Angiotensin II-induced phosphorylation of proteins was examined in isolated myocytes from hearts of Dahl rats. A high salt diet induced cardiac hypertrophy in Dahl salt-sensitive rats. Angiotensin II-induced phosphorylation of a 42-kd protein (pp42) was detected by two-dimensional electrophoresis in hypertrophic but not normal ventricular myocytes. Angiotensin II stimulation was time-dependent, with a peak effect at 30 minutes. The half-maximal and maximal concentrations of angiotensin II that stimulated pp42 phosphorylation were 1 and 10 nM, respectively. Phosphorylation of pp42 was a function of cardiac hypertrophy. Phorbol 12-myristate 13-acetate-induced phosphorylation of pp42 indicates the possibility of an association between protein kinase C and the signal transduction pathway of angiotensin II-induced pp42 phosphorylation. Ionomycin and A23187 (both at 1 microM) did not stimulate phosphorylation of pp42. Angiotensin II produced a small increase in the synthesis of myocyte proteins in both normal and hypertrophic cells as shown by [35S]methionine incorporation. However, this increase could not account for the increase in the phosphate content of pp42. This protein was not an isoform of actin nor was it of platelet origin. These results raise the possibility that angiotensin II may play a role in the activation of factors in hypertrophic myocytes; however, further study is required to define a link between phosphorylation of pp42 and the hypertrophic process.
在 Dahl 大鼠心脏分离的心肌细胞中检测了血管紧张素 II 诱导的蛋白质磷酸化。高盐饮食可诱导 Dahl 盐敏感大鼠发生心脏肥大。通过二维电泳在肥大的而非正常的心室肌细胞中检测到血管紧张素 II 诱导的一种 42-kd 蛋白（pp42）的磷酸化。血管紧张素 II 的刺激具有时间依赖性，在 30 分钟时达到峰值效应。刺激 pp42 磷酸化的血管紧张素 II 的半最大浓度和最大浓度分别为 1 和 10 nM。pp42 的磷酸化是心脏肥大的一个函数。佛波酯 12-肉豆蔻酸酯 13-乙酸酯诱导的 pp42 磷酸化表明蛋白激酶 C 与血管紧张素 II 诱导的 pp42 磷酸化信号转导途径之间存在关联的可能性。离子霉素和 A23187（均为 1 μM）未刺激 pp42 的磷酸化。如 [35S]甲硫氨酸掺入所示，血管紧张素 II 在正常和肥大细胞中均使心肌细胞蛋白合成略有增加。然而，这种增加并不能解释 pp42 磷酸含量的增加。该蛋白既不是肌动蛋白的同工型，也不是血小板来源的。这些结果增加了血管紧张素 II 可能在肥大心肌细胞中激活因子中起作用的可能性；然而，需要进一步研究来确定 pp42 磷酸化与肥大过程之间的联系。
