[内皮素和蛋白激酶C对βA(4)25 - 35在皮肤微血管的血管活性机制的影响]
[The effect of endothelin and protein kinase C on the vasoactive mechanisms of beta A(4)25-35 at skin microvasculature].
作者信息
Chen H, Khalil Z, Helme R D
机构信息
Department of Neurology, Beijing Hospital.
出版信息
Zhonghua Yi Xue Za Zhi. 1997 May;77(5):367-70.
OBJECTIVE
The aim of the present study is to investigate the mechanisms of beta A(4)25-35 at the level of skin microvascula ture.
METHODS
Using a blister model in rat skin, we examined the possibilities that beta A(4)25-35 induces VC effect via the release of endothelin and the involvement of protein kinase C (PKC). Changes in microvascular blood flow were monitored using laser Doppler flowmetry and the area within the response curve measured.
RESULTS
The results showed that either the endothelin receptor antagonist (BQ--123 at 10 mumol) or PKC inhibitor (bisindolylmaleimide at 1 mu mol) was perfused before beta A(4)25-35. It prevented beta A(4)25-35 from inducing a VC effect and allowed a subsequent SP to induce a normal response.
CONCLUSION
Both endothelin and PKC play a role in the mechanism be which beta A(4)25-35 induces VC effect and modulates subsequent SP response at the level of skin microvasculature. We suggest the possibility that the vascular activity of beta A(4)25-35 could be mediated via endothelin with subsequent activation of PKC.
目的
本研究旨在探讨βA(4)25 - 35在皮肤微血管水平的作用机制。
方法
利用大鼠皮肤水疱模型，我们研究了βA(4)25 - 35通过内皮素释放及蛋白激酶C（PKC）参与诱导血管收缩（VC）效应的可能性。使用激光多普勒血流仪监测微血管血流变化并测量反应曲线内的面积。
结果
结果显示，在给予βA(4)25 - 35之前灌注内皮素受体拮抗剂（10 μmol的BQ - 123）或PKC抑制剂（1 μmol的双吲哚马来酰胺），可防止βA(4)25 - 35诱导VC效应，并使随后的P物质（SP）诱导正常反应。
结论
内皮素和PKC在βA(4)25 - 35诱导VC效应及调节皮肤微血管水平随后的SP反应机制中均起作用。我们认为βA(4)25 - 35的血管活性可能通过内皮素介导，随后激活PKC。
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