尾加压素Ⅱ对血管平滑肌细胞增殖的影响

目的研究体内新发现的缩血管活性肽尾加压素Ⅱ（ｕｒｏｔｅｎｓｉｎ Ⅱ， Ｕ Ⅱ）对大鼠主动脉平滑肌细胞增殖作用的影响以及ＵⅡ作用的细胞内信号转导机制。方法在培养的大鼠主动脉平滑肌细胞（ＡＳＭＣ）上，采用［３Ｈ］－胸腺嘧啶（［３Ｈ］－ＴｄＲ）参入法，观察 ＵⅡ对细胞 ＤＮＡ合成的刺激作用；加入不同的细胞内信号转导阻断剂，观察对ＵⅡ效应的影响。结果 Ｉ× １０－９～ １× １０－７ ｍｏｌ·Ｌ－１ ＵⅡ以浓度依赖方式促进 ＡＳＭＣ［３Ｈ］－ＴｄＲ参入增加， １× １０－９、１× １０－８和 １×１０－７ｍｏｌ·Ｌ－１ＵⅡ组［３Ｈ］－ＴｄＲ参入量分别较对照组增加２２％（Ｐ＜０．０５），５７％（Ｐ＜０，０１）和６５％（Ｐ＜０．０１）。ＵⅡ的效应能被钙通道阻断剂尼卡地平、ＰＫＣ阻断剂Ｈ７、钙调素激酶（ＣａＭ－ＰＫ）阻断剂 Ｗ７和 ＭＡＰＫ阻断剂 ＰＤ９８０５９所阻断，抑制率分别为５５％（Ｐ＜０．０１），２７％（Ｐ＜０．０１），１８％（Ｐ＜０．０５）和１６％（Ｐ＜０．０５）。结论 ＵⅡ是一种新发现的强烈的促ＡＳＭＣ增生的内源性丝裂原，其促丝裂效应可能通过Ｃａ２＋、ＰＫＣ、ＣａＭ－ＰＫ和ＭＡＰＫ来介导。

Stimulating proliferation of aorta smooth muscle cells of rat by rat urotensin

AIM　To investigate effect of urotensin Ⅱ (UⅡ)on proliferation of aort a smooth muscle cells （ASMC）of rat and study the signal transduction pathway o f it. METHODS　In cultured ASMC of rat, UⅡ was used to stimulate proliferation of these cells and levels of ［3H］-TdR incorporation were used to evaluate the speed of DNA synthesis, and different inhibitors were used to s tudy the action of different signal transduction pathway of mitogenic effect of UⅡ on VSMC. RESULTS　1×10-9～1×10-7 mol*L- 1 UⅡ caused marked concentration-dependent increasing of ［3H］-TdR i ncor poration of ASMC. ［3H］-TdR incorporation of 1×10-9,1×10-8 and 1×10-7 mol*L-1 UⅡ were 22%（P<0.05）, 57%（P<0.01）and 65%（P<0.01）higher than control. Nicardipine, H7, W7 and PD98059 , which are inhibitors of calcium channel, PKC, CaM-PK and MAPK respectively, inhibited the effects of UⅡ obviously, with the inhibitory rate by 55%（P< 0.01）, 27%（P<0.01）,18%（P<0.05）and 16%（P<0.05）respectively . CONCLUSION　UⅡ is a strong mitogen for VSMC and the mitogenic e ffect of UⅡ is probably mediated by Ca2+, PKC, CaM-PK and MAPK signal tr ansduction pathway.