降钙素基因相关肽对尾加压素Ⅱ诱导的血管平滑肌增殖的影响

目的 :观察降钙素基因相关肽 (CGRP)对尾加压素Ⅱ (UrotensionⅡ ,UⅡ )刺激的血管平滑肌细胞 (VSMC)增殖的影响及机制。方法 :贴块法培养大鼠胸主动脉VSMC ;3 H -胸腺嘧啶 (3 H -TdR)掺入测定VSMCDNA合成 ;γ- 3 2 P -ATP标记的同位素法测定丝裂素活化蛋白激酶 (MAPK)活性。结果 :UⅡ (10 -8mol/L)显著促进VSMC3 H -TdR掺入和激活MAPK。与对照组比较 ,分别增加 4 8%和 2 2 6 % (P <0 .0 1)。CGRP有效抑制UⅡ诱导的VSMC3 H -TdR掺入和MAPK激活。与UⅡ组比较 10 -9、10 -8、10 -7mol/LCGRP分别使VSMC3 H -TdR掺入降低 18%、2 5 %和31% (P <0 .0 1) ,使MAPK活性分别降低 2 6 %、5 0 %和 6 4 % (P <0 .0 1)。结论 :CGRP抑制UⅡ诱导的VSMC增殖 ,其机制可能与CGRP拮抗UⅡ刺激的MAPK活性有关

Effects of calcitonin gene related peptide on proliferation of vascular smooth muscle cells induced by urotensin Ⅱ

Objective To observe the effects and the potential mechanism of calcitonin gene related peptide (CGRP) on proliferation of vascular smooth muscle cells (VSMC) induced by urotensin Ⅱ (UⅡ).Methods Culture of rat aortic VSMC. DNA synthesis of VSMC was measured by 3 H-TdR incorporation. Mitogen activated protein kinase (MAPK) activities were determined by isotope tagged with γ- 32 P-ATP. Results UⅡ(10 -8 mol/L) significantly elevated 3 H-TdR incorporation and MAPK activation of VSMC, increased by 48% ( P <0.01) and 226% respectively ( P <0.01) compared with control group.CGRP obviously inhibited proliferation of VSMC induced by UⅡ.Compared with UⅡ group, 10 -9 ?10 -8 ?10- 7 mol/L CGRP decreased 3 H-TdR incorporation of VSMC by 18%?25%和31%( P <0.01),and MAPK activities by 26%?50%和64%( P <0.01)respectively.Conclusion CGRP inhibits proliferation of VSMC induced by UⅡ and the mechanism could be involved in antagonistic role of CGRP against MAPK activation induced by UⅡ.