Role of Calcium ion in vascular smooth muscle and the alteration by aging.

(1)血管紧张素II诱导大鼠主动脉血管平滑肌细胞发生钙瞬变。在老年大鼠的细胞中减弱这种反应。(2)在器官浴中安装主动脉条，记录所产生的张力。血管紧张素II可增强血管紧张素的收缩作用，此作用可被L型钙通道阻滞剂维拉帕米、酪氨酸激酶抑制剂金雀异黄素、浓度依赖性地抑制谷氨酰胺引起的收缩所抑制。MA激酶/ERK激酶抑制剂PD98059对血管收缩无明显影响，提示血管紧张素诱导的血管收缩作用与酪氨酸激酶有关，而与MAPKase无关。(3)老年大鼠的血管收缩作用减弱。然而，竞争性RT-PCR检测到的血管紧张素II受体的表达水平并没有随着年龄的增长而改变。此外，血管紧张素受体在老年心脏中的表达没有减少。血管紧张素反应的年龄相关性改变可能是由于受体刺激后信号通路的改变。

(1) Angiotensin II induced Ca transient in cultured vascular smooth muscle cells dereived from rat aorta. The response was attenuated in cells from aged rat.(2) Aortic strip was mounted in the organ bath and the developed tension was recorded. Angiotensin II increased the force of contraction, and the response was inhibited by L-type Ca channel blocker, verapamil, Tyrosine kinase inhibitor, gen istein, con centration-depend ently inhibited the ani gotensin-induced contraction. MA kinase/ERK kinse inhibitor, PD9 8059, did not affect on the contraction, suggesting that the tyrosine kin ase, but not MAP kin ase, is involved in the angiotensin -indu ced vas ocon striction.(3) Angiotensin-induced vasoconstriction was attenuated in the aged rat aorta. However, the level of expression of angiotensin II receptor, which was determined by competitive RT-PCR, was not altered by aging. In addition, the expression of angiotensin receptor was not reduced in the aged heart. The age- related change in response to angiotensin may be due to alteration of signaling pathway after the receptor stimulation.