Calcium-activated chloride channels are involved in two-phase hypoxic pulmonary vasoconstriction in rat pulmonary arteries.
- Author:
Lei YING
1
,
2
,
3
;
Hai-Xia YAO
;
Lin-Jing HUANG
;
Ying-Chun MA
;
Jin-Bo HE
;
Dan CHEN
;
Hai-E CHEN
;
Yang WANG
;
Wan-Tie WANG
Author Information
1. Department of Pathophysiology
2. Institute of Ischemia-reperfusion Injury, Wenzhou Medical University, Wenzhou 325035, China
3. Department of Anesthesiology, The Sixth People's Hospital of Shanghai, Shanghai 200233, China. wzwwt@tom.com.
- Publication Type:Journal Article
- MeSH:
Animals;
Chloride Channels;
physiology;
Glycolates;
pharmacology;
Hypoxia;
physiopathology;
Male;
Norepinephrine;
pharmacology;
Pulmonary Artery;
physiopathology;
Rats;
Rats, Sprague-Dawley;
Vasoconstriction;
Vasodilation
- From:
Acta Physiologica Sinica
2014;66(2):203-209
- CountryChina
- Language:Chinese
-
Abstract:
The aim of the present study was to investigate the roles of calcium-activated chloride channels (Cl(Ca)) in the two-phase hypoxic pulmonary vasoconstriction (HPV). The second pulmonary artery branches were dissected from male Sprague-Dawley rats, and the changes in vascular tone were measured by using routine blood vascular perfusion in vitro. The result showed that, under normoxic conditions, Cl(Ca) inhibitors (NFA and IAA-94) significantly relaxed second pulmonary artery contracted by norepinephrine (P < 0.01), but merely had effects on KCl-induced second pulmonary artery contractions. A biphasic contraction response was induced in second pulmonary artery ring pre-contracted with norepinephrine exposed to hypoxic conditions for at least one hour, but no biphasic contraction was observed in pulmonary rings pre-contracted with KCl. NFA and IAA-94 significantly attenuated phase II sustained hypoxic contraction (P < 0.01), and also attenuated phase I vasodilation, but had little effect on phase I contraction. These results suggest that Cl(Ca) is an important component forming phase II contraction in secondary pulmonary artery, but not involved in phase I contraction.
