Angiostensin II (Ang II) regulates the migration and proliferation of vascular smooth muscle cells. Recent studies indicate that intermediate-conductance Ca2+ -activated K+ (IKca) channels have an important role in cell migration and proliferation. It is not known, however, whether the action of Ang II is linked to IKca channel regulation. Here, we investigated the modulation of IKca channels by Ang II in artery smooth muscle cells. Functional IKca channel expression in cultured embryonic rat aorta smooth muscle (A10) cells was studied using the patch-clamp technique. These cells predominantly express IKca channels. In contrast, large-conductance Ca2+ -activated K+ (BKca) currents were rarely observed in excised patches. Ang II increased the IKca current in a contration-dependent manner. Losartan (1.0 microM), an AT1 selective antagonist, abolished the activation of IKca channels by Ang II. Pretreatment with 100 microM myristoylated protein kinase C inhibitor peptide 20-28 or 10 microM GF109203X completely abolished the AngII-induced activation of IKca currents, whereas the action of Ang II was not prevented in the presence of 100 microM Rp-cyclic 3', 5'-hydrogen phosphotiate adenosine triethylammonium, a protein kinase A inhibitor, or 1.0 microM KT-5823, a protein kinase G inhibitor. A membrane permeant analogue of diacylglycerol 1, 2-dioctanoyl-sn-glycerol (10 microM) induced the activation of IKca currents. These data suggest that Ang II activates IKca channels through the activation of protein kinase C, and the AT1 receptor is involved in the regulation of these channels.

译文

Angiostensin II (Ang II) 调节血管平滑肌细胞的迁移和增殖。最近的研究表明,中间电导Ca2激活的K (IKca) 通道在细胞迁移和增殖中起重要作用。但是,尚不清楚Ang II的作用是否与IKca通道调节有关。在这里,我们研究了Ang II对动脉平滑肌细胞中IKca通道的调节。使用膜片钳技术研究了培养的胚胎大鼠主动脉平滑肌 (A10) 细胞中功能性IKca通道的表达。这些细胞主要表达IKca通道。相反,在切除的贴片中很少观察到大电导Ca2激活的K (BKca) 电流。Ang II以依赖于收缩的方式增加了IKca电流。氯沙坦 (1.0 microM),一种AT1选择性拮抗剂,通过Ang II消除了IKca通道的激活。用100 microM肉豆蔻酰化蛋白激酶C抑制剂肽20-28或10 microM GF109203X进行预处理完全消除了AngII诱导的IKca电流的激活,而在存在100 microM Rp-环状3 ',5'-磷酸氢腺苷三乙基铵的情况下,Ang II的作用没有被阻止,蛋白激酶a抑制剂,或1.0 microM KT-5823,蛋白激酶G抑制剂。二酰基甘油1,2-二酰基-sn-甘油 (10 microM) 的膜渗透类似物诱导了IKca电流的激活。这些数据表明Ang II通过激活蛋白激酶C激活IKca通道,AT1受体参与了这些通道的调节。

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