Role of calcium-activated chloride channels in the regulation of pulmonary vascular tone in rats.
- Author:
Zhao YANG
1
;
Zhen-Xiang ZHANG
;
Yong-Jian XU
;
Tao YE
;
Ya-Qing LI
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Calcium; physiology; Chloride Channels; physiology; Glycolates; pharmacology; Male; Muscle, Smooth, Vascular; physiology; Niflumic Acid; pharmacology; Phenylephrine; pharmacology; Pulmonary Artery; physiology; Rats; Rats, Sprague-Dawley; Vasoconstriction
- From: Chinese Journal of Applied Physiology 2006;22(2):215-218
- CountryChina
- Language:Chinese
-
Abstract:
AIMTo investigate the role of calcium-activated chloride channels and the Cl- channel blockers niflumic acid (NFA) and indanyloxyacetic acid (IAA-94) in the regulation of vascular contraction induced by phenylephrine (PE).
METHODSThe PE-induced contraction in rat pulmonary artery was observed by using routine blood vascular perfusion in vitro. The fluorescence Ca2+ indicator Fura-2/AM was used to observe intracellular free Ca2+ concentration ([Ca2+]i) of rat pulmonary artery smooth muscle cells (PASMCs) which were obtained by the acute enzyme separation method (collagenase I plus papain) on NFA and IAA-94 effects on PE-induced contraction. Changes of [Ca2+]i in PASMCs were measured by spectrofluorometry.
RESULTSThe anion channel blockers NFA and IAA-94 produced inhibitory effects on PE-induced contractions in the pulmonary artery. NFA and IAA-94 negligibly affected the KCl-induced pulmonary artery contractions. PE could increase [Ca2+]i but NFA and IAA-94 negligibly affected it.
CONCLUSIONCalcium-activated chloride channels contribute to the agonist-induced pulmonary artery contractions under physiological conditions, which may be a new clue to investigate the hypoxic pulmonary vasoconstriction.
