Henrion D, Laher I, Laporte R, Bevan J A
Department of Pharmacology, University of Vermont, College of Medicine, Burlington 05405-0068.
Eur J Pharmacol. 1992 Nov 24;224(1):13-20. doi: 10.1016/0014-2999(92)94812-a.
Angiotensin II (AII, 0.1 nM) increased concentration dependently the sensitivity of rabbit aortic rings to low concentrations of noradrenaline. This was not associated with increases in noradrenaline-induced 45Ca2+ uptake or efflux and was prevented by the protein kinase C (PKC) inhibitors staurosporine (0.01 microM) and calphostin C (0.1 microM). Pretreatment of the rings with PMA (phorbol-12-myristate-13-acetate, 0.1 and 1 microM, 24 h at 4 degrees C) abolished the potentiation phenomenon. We conclude that AII potentiation of noradrenaline-induced vascular tone may be due to a PKC-mediated increase in intracellular sensitivity of the contractile apparatus to Ca2+.
血管紧张素II（AII，0.1纳摩尔）浓度依赖性地增加了兔主动脉环对低浓度去甲肾上腺素的敏感性。这与去甲肾上腺素诱导的45Ca2+摄取或流出增加无关，并被蛋白激酶C（PKC）抑制剂星形孢菌素（0.01微摩尔）和钙磷蛋白C（0.1微摩尔）所阻断。用佛波醇-12-肉豆蔻酸酯-13-乙酸酯（PMA，0.1和1微摩尔，4℃下24小时）预处理主动脉环可消除增强现象。我们得出结论，AII对去甲肾上腺素诱导的血管张力的增强作用可能是由于PKC介导的收缩装置对Ca2+的细胞内敏感性增加所致。
