蛋白激酶C在血管平滑肌反应放大中的调节作用。

Blood vessels Pub Date : 1990-01-01 DOI:10.1159/000158827
I Laher, L P Thompson, L Gagne
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引用次数: 24

摘要

在兔股动脉环中研究了α -肾上腺素受体介导的血管紧张素II对血管收缩的扩增作用。血管紧张素II的阈值浓度(0.1 nM)使对可乐定的最大反应增加到对照的139 +/- 8%,敏感性增加3.2倍。当组织用staurosporine(一种蛋白激酶c的抑制剂)预处理时,血管紧张素II的这些作用被逆转。血管紧张素II对α -肾上腺素介导的凝血酶和去甲肾上腺素的血管收缩作用的放大也被staurosporine预处理逆转。血管紧张素II诱导血管平滑肌的反应放大是一种非特异性现象,暗示细胞内换能器系统的受体后相互作用。我们的研究结果表明,当血管紧张素II激活蛋白激酶C时,动脉对α -肾上腺素受体激动剂的反应被放大。这提供了血管敏感性的非特异性变化,通过已知的调节Ca2(+)依赖性现象的酶系统的突触后调节的强直性改变,例如那些与血管兴奋-收缩机制相关的现象。
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Protein kinase C as a modulator of response amplification in vascular smooth muscle.

The amplification of alpha-adrenoceptor-mediated vasoconstriction by angiotensin II was studied in femoral artery rings from rabbits. Threshold concentrations of angiotensin II (0.1 nM) increased the maximal response to clonidine to 139 +/- 8% of control and produced a 3.2-fold increase in sensitivity. These effects of angiotensin II were reversed when tissues were pretreated with staurosporine (50 nM), an inhibitor of protein kinase C. The amplification of the alpha-adrenoceptor-mediated vasoconstrictor effects of thrombin and norepinephrine by angiotensin II were also reversed by pretreatment with staurosporine. Angiotensin II induced a response amplification in vascular smooth muscle known to be a nonspecific phenomenon, implying postreceptor interaction at intracellular transducer systems. Our findings suggest that upon activation of protein kinase C by angiotensin II, arterial responses to alpha-adrenoceptor agonists are amplified. This provides for nonspecific changes in vascular sensitivity by tonic alterations in postsynaptic modulation by enzyme systems known to regulate Ca2(+)-dependent phenomena, e.g. those related to vascular excitation-contraction mechanisms.

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