Factors responsible for acetylcholine-induced dilatation in the isolated perfused rat kidney

General Pharmacology-the Vascular System Pub Date : 2000-03-01 DOI:10.1016/S0306-3623(00)00058-6

Ilknur Ay, Selda Emre, Meral Tuncer

{"title":"Factors responsible for acetylcholine-induced dilatation in the isolated perfused rat kidney","authors":"Ilknur Ay, Selda Emre, Meral Tuncer","doi":"10.1016/S0306-3623(00)00058-6","DOIUrl":null,"url":null,"abstract":"<div>Mechanism of acetylcholine (ACh)-induced dilatation was investigated in isolated perfused rat kidney. Under a constant flow of 8–10 ml/min, ACh (0.001–3 μg/0.1 ml) caused a dose-dependent decrease in perfusion pressure raised by submaximum concentration of phenylephrine (PE). ACh-induced dilatations were inhibited by atropine (10−6 mol/l), hexamethonium (10−4 mol/l), indomethacin (10−5 mol/l), methylene blue (10−5 mol/l), NG-nitro-l-arginine (l-NOARG, 10−4 mol/l), tetrodotoxin (TTX, 10−6 mol/l), capsaicin (10−6 mol/l), and glibenclamide (10−5 mol/l). These results suggest that in the isolated perfused rat kidney, endothelium-derived hyperpolarizing factor (EDHF), nitric oxide (NO), and tachykinin neuromediators may play a role in ACh-induced dilatation via stimulation of guanylate cyclase and opening of ATP-sensitive potassium channels.</div>","PeriodicalId":12607,"journal":{"name":"General Pharmacology-the Vascular System","volume":"34 3","pages":"Pages 175-181"},"PeriodicalIF":0.0000,"publicationDate":"2000-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0306-3623(00)00058-6","citationCount":"5","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"General Pharmacology-the Vascular System","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0306362300000586","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}

引用次数: 5

Abstract

Mechanism of acetylcholine (ACh)-induced dilatation was investigated in isolated perfused rat kidney. Under a constant flow of 8–10 ml/min, ACh (0.001–3 μg/0.1 ml) caused a dose-dependent decrease in perfusion pressure raised by submaximum concentration of phenylephrine (PE). ACh-induced dilatations were inhibited by atropine (10⁻⁶ mol/l), hexamethonium (10⁻⁴ mol/l), indomethacin (10⁻⁵ mol/l), methylene blue (10⁻⁵ mol/l), N^G-nitro-l-arginine (l-NOARG, 10⁻⁴ mol/l), tetrodotoxin (TTX, 10⁻⁶ mol/l), capsaicin (10⁻⁶ mol/l), and glibenclamide (10⁻⁵ mol/l). These results suggest that in the isolated perfused rat kidney, endothelium-derived hyperpolarizing factor (EDHF), nitric oxide (NO), and tachykinin neuromediators may play a role in ACh-induced dilatation via stimulation of guanylate cyclase and opening of ATP-sensitive potassium channels.

查看原文本刊更多论文

乙酰胆碱诱导离体灌注大鼠肾脏扩张的相关因素

探讨乙酰胆碱(ACh)诱导大鼠离体肾扩张的机制。在8 ~ 10 ml/min恒定流速下，ACh (0.001 ~ 3 μg/0.1 ml)可引起苯基肾上腺素(PE)亚最大浓度引起的灌注压呈剂量依赖性降低。阿托品(10−6 mol/l)、六甲铵(10−4 mol/l)、吲哚美辛(10−5 mol/l)、亚甲基蓝(10−5 mol/l)、ng -硝基-l-精氨酸(l- noarg, 10−4 mol/l)、河河鱼毒素(TTX, 10−6 mol/l)、辣椒素(10−6 mol/l)和格列本脲(10−5 mol/l)均可抑制乙酰胆碱诱导的扩张。这些结果表明，在离体灌注大鼠肾脏中，内皮源性超极化因子(EDHF)、一氧化氮(NO)和速激肽神经介质可能通过刺激鸟苷酸环化酶和打开atp敏感钾通道，在乙酰胆碱诱导的扩张中发挥作用。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文求助全文

来源期刊

General Pharmacology-the Vascular System

自引率

0.00%

发文量