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血管紧张素II对离体蟾蜍皮肤电特性的刺激作用。

Stimulatory effect of angiotensin II on the electric properties of the isolated toad skin.

作者信息

Norris B, Concha J, Contreras G, González C

机构信息

Department of Physiological Sciences, Faculty of Biological and Natural Sciences, University of Concepción, Chile.

出版信息

Biochem Pharmacol. 1988 Aug 1;37(15):3005-9. doi: 10.1016/0006-2952(88)90289-4.

Abstract

In 1982 we showed that angiotensin II (Agt II) stimulates the bioelectric properties of the isolated toad skin and that this effect is blocked by pretreatment of the skin with indomethacine [J. B. Concha et al., IRCS Med. Sci. 10, 584 (1982)]. Ussing's technique and several inhibitors were used to continue this study on the isolated Pleurodema thaul skin. Serosal Agt II produced a dose-dependent increase in electrical parameters: a maximal concentration of 6 X 10(-6) M Agt II increased potential difference by 43 +/- 7.8% and short-circuit current by 51.5 +/- 7.7%. The responses were not affected by either alpha or beta blockers or by atropine. Indomethacine blocked responses to the calcium ionophore A23187 and to Agt II which were similar to each other. Additive effects of Agt II and of the calcium ionophore A23187 were found. No response to Agt II was obtained when Ca2+-free Ringer was used on the serosal side. Calcium channel blockers (nifedipine, verapamil, manganese), pentobarbitone and saralasin blocked the response to Agt II. This pharmacological evidence is in favour of the hypothesis that Agt II activates specific membrane receptors, leading to Ca2+ release and formation of prostaglandins which stimulate adenyl cyclase. This increases cAMP secretion, which in turn increases apical membrane permeability to sodium and enhances the active transport system.

摘要

1982年我们发现,血管紧张素II(Agt II)可刺激离体蟾蜍皮肤的生物电特性,且用吲哚美辛预处理皮肤可阻断此效应[J. B. 康查等人,《医学研究委员会通报》10, 584 (1982)]。运用乌斯电极技术和几种抑制剂继续对离体的南方雨蛙皮肤进行此项研究。浆膜侧的Agt II使电参数呈剂量依赖性增加:Agt II最大浓度为6×10(-6) M时,电位差增加43±7.8%,短路电流增加51.5±7.7%。这些反应不受α或β受体阻滞剂或阿托品的影响。吲哚美辛可阻断对钙离子载体A23187和对Agt II的反应,二者反应相似。发现Agt II与钙离子载体A23187有相加效应。当浆膜侧使用无钙林格液时,未获得对Agt II的反应。钙通道阻滞剂(硝苯地平、维拉帕米、锰)、戊巴比妥和沙拉新可阻断对Agt II的反应。这一药理学证据支持如下假说:Agt II激活特定膜受体,导致钙离子释放并形成前列腺素,进而刺激腺苷酸环化酶。这会增加环磷酸腺苷(cAMP)分泌,进而增加顶端膜对钠的通透性并增强主动转运系统。

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