Vasodilation effect of atropine on rat mesenteric artery.
- Author:
Jian-pu ZHENG
1
;
Yong-xiao CAO
;
Cang-bao XU
;
Lars EDVINSSON
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Atropine; pharmacology; Calcium; metabolism; Calcium Chloride; antagonists & inhibitors; Cyclooxygenase Inhibitors; pharmacology; Endothelial Cells; physiology; Female; In Vitro Techniques; Indomethacin; antagonists & inhibitors; Male; Mesenteric Artery, Superior; drug effects; NG-Nitroarginine Methyl Ester; antagonists & inhibitors; Nitric Oxide Synthase; antagonists & inhibitors; Norepinephrine; antagonists & inhibitors; Potassium Chloride; antagonists & inhibitors; Rats; Rats, Sprague-Dawley; Vasodilation; drug effects; Vasodilator Agents; pharmacology
- From: Acta Pharmaceutica Sinica 2005;40(5):402-405
- CountryChina
- Language:Chinese
-
Abstract:
AIMTo study the vasodilation effect of atropine and its mechanism.
METHODSIsometric tension was recorded in isolated rat super mesenteric arteries precontracted by noradrenaline (NE) to study the vasodilation effect of atropine, and to investigate the role of endothelial cell and vascular smooth muscle cell on vasodilation.
RESULTSAtropine was shown to significantly dilate the endothelium-intact and endothelium-denuded arteries precontracted by NE. Nomega-Nitro-L-arginine methyl ester (L-NAME, nitric oxide synthase inhabitor), indomethacin (cyclooxygenase inhibitor), propranolol (general beta adrenoceptor antagonist) and glibenclamide (ATP sensitive potassium channel inhibitor) showed no effect on vasodilation of atropine. Atropine did not affect the concentration-contraction curve of K+. However, atropine suppressed the contraction induced by NE and CaCl2, but not that by caffeine in the Ca+ -free Krebs solution.
CONCLUSIONAtropine showed significant vasodilation effect which may derive, in part, from endothelium. Besides, atropine could inhibit the receptor-mediated Ca2+ -influx and Ca2+ -release, which was inferred to the mechanism of atropine on vasodilation.
