Oike M, Takahashi N, Ito Y
Department of Pharmacology, Faculty of Medicine, Kyushu University, Fukuoka, Japan.
Biochem Biophys Res Commun. 1996 May 15;222(2):208-14. doi: 10.1006/bbrc.1996.0723.
We observed the effects of angiotensin II (AII) on the contractile response and the Ca2+ transient induced by high K+ solution in the rabbit mesenteric artery. In the control condition, the repeated application of high K+ solution with 90 min interval induced a gradually increasing contraction, which was accompanied with a significant elevation of the intracellular calcium concentration ([Ca2+]i). Treatment of the tissue with AII for one to two hours abolished the incremental response of the contraction. The change in [Ca2+]i induced by high K+ solution, however, was not significantly different with and without treatment with AII. Pretreatment of the tissue with actinomycin D abolished the inhibitory action of AII on the incremental contraction, indicating the involvement of a transcriptional process. These results indicate that AII impairs vascular contractility through the modulation of Ca(2+)-sensitivity of the contractile machinery.
我们观察了血管紧张素II（AII）对家兔肠系膜动脉中高钾溶液诱导的收缩反应和Ca2+瞬变的影响。在对照条件下，以90分钟的间隔重复应用高钾溶液会诱导逐渐增强的收缩，同时伴随着细胞内钙浓度（[Ca2+]i）的显著升高。用AII处理组织一到两小时消除了收缩的递增反应。然而，无论是否用AII处理，高钾溶液诱导的[Ca2+]i变化并无显著差异。用放线菌素D预处理组织消除了AII对递增收缩的抑制作用，表明涉及转录过程。这些结果表明，AII通过调节收缩机制的Ca(2+)敏感性来损害血管收缩性。
