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离体灌注犬肠系膜动脉对ATP血管收缩反应的药理学分析。

Pharmacological analysis of vasoconstrictor responses to ATP of isolated, perfused dog mesenteric arteries.

作者信息

Chiba S, Tsukada M

出版信息

Arch Int Pharmacodyn Ther. 1986 May;281(1):79-88.

PMID:3753099
Abstract

The stainless steel cannula inserting method was used to analyze the characteristics of the vasoconstriction induced by ATP in isolated, perfused dog mesenteric arteries. A dose of 100-1000 micrograms of ATP induced vasoconstriction. It was produced repetitively at 20-min intervals. The vasoconstriction was not modified by phentolamine in doses which completely inhibited norepinephrine-induced vasoconstriction. Aminophylline significantly suppressed ATP-induced vasoconstrictions. KCl-induced vasoconstriction was significantly depressed by a potent Ca antagonist, diltiazem. ATP-induced vasoconstriction was also significantly suppressed by diltiazem but to a lesser degree. ATP-induced vasoconstriction was not significantly suppressed by 30 and 100 micrograms of dipyridamole. After treatment with intraluminal saponin (0.3-3 mg) which caused a disappearance of the vascular endothelium, the ATP-induced vasoconstrictor response was significantly enhanced. From these results it is concluded that ATP-induced vasoconstriction may be mediated via P1-purinoceptors and be partially due to increases in activation of Ca inward current.

摘要

采用不锈钢套管插入法分析三磷酸腺苷(ATP)对离体灌注犬肠系膜动脉血管收缩作用的特点。剂量为100 - 1000微克的ATP可引起血管收缩。这种作用每隔20分钟重复出现一次。能完全抑制去甲肾上腺素引起的血管收缩的酚妥拉明剂量,对ATP引起的血管收缩无影响。氨茶碱能显著抑制ATP引起的血管收缩。氯化钾引起的血管收缩可被强效钙拮抗剂地尔硫卓显著抑制。地尔硫卓也能显著抑制ATP引起的血管收缩,但抑制程度较小。30微克和100微克双嘧达莫对ATP引起的血管收缩无显著抑制作用。在用腔内皂苷(0.3 - 3毫克)处理导致血管内皮消失后,ATP引起的血管收缩反应显著增强。从这些结果可以得出结论,ATP引起的血管收缩可能通过P1 - 嘌呤受体介导,部分原因是钙内向电流激活增加。

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