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

(1)血管紧张素II诱导培养大鼠主动脉血管平滑肌细胞钙瞬变。老年大鼠细胞的反应减弱。(2)将主动脉条置于脏器浴中，记录血管张力变化情况。血管紧张素II增加收缩力，l型Ca通道阻滞剂、维拉帕米、酪氨酸激酶抑制剂、根司因抑制收缩力，浓度依赖性地抑制血管紧张素诱导的收缩。MA激酶/ERK激酶抑制剂pd98059对血管收缩无影响，提示酪氨酸kin酶而非MAP kin酶参与血管紧张素诱导的输精管收缩。(3)老龄大鼠主动脉血管紧张素诱导的血管收缩减弱。然而，竞争性RT-PCR检测血管紧张素II受体的表达水平不随年龄的增长而改变。此外，老年心脏血管紧张素受体的表达不降低。血管紧张素反应的年龄相关性变化可能与受体刺激后信号通路的改变有关。

(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.