Effect of ischemia/hypoxia on mesenteric vasomotor function in spontaneously hypertensive rats and its possible mechanism.
- Author:
Ming ZHAO
1
;
Xiao-Jiang YU
;
Hong-Li ZHANG
;
Xue-Yuan BI
;
Hao HU
;
Wei-Jin ZANG
Author Information
1. Department of Pharmacology, School of Medicine, Xi'an Jiaotong University, Xi'an 710061, China.
- Publication Type:Journal Article
- MeSH:
Animals;
Calcium;
metabolism;
Endothelium, Vascular;
metabolism;
physiopathology;
Hypertension;
physiopathology;
Hypoxia;
physiopathology;
In Vitro Techniques;
Male;
Mesenteric Arteries;
physiopathology;
Muscle, Smooth, Vascular;
physiopathology;
Nitric Oxide;
biosynthesis;
Rats;
Rats, Inbred SHR;
Rats, Inbred WKY;
Vasomotor System;
physiopathology
- From:
Acta Physiologica Sinica
2011;63(6):540-548
- CountryChina
- Language:Chinese
-
Abstract:
Hypertension is a common cardiovascular disease and can induce many complications, such as stroke and coronary heart disease. The purpose of the present study was to investigate the effect of ischemia/hypoxia on mesenteric artery vasomotor function in spontaneously hypertensive rats (SHR). Rat mesenteric arterial rings were cultured in modified ischemia-mimetic solution in a hypoxia incubator for a certain time period. Isometric tension changes of isolated mesenteric arterial rings were recorded continuously by a myograph system. The results obtained were as follows: In SHR group, the maximum contractions to KCl and phenylephrine (PE) were increased, and the maximum relaxation to acetylcholine (ACh) was decreased, compared to those in Wistar-Kyoto (WKY) rats group. Compared with SHR group and WKY with acute ischemia/hypoxia (WKY+H) group, SHR with acute ischemia/hypoxia (SHR+H) increased the maximum contractions induced by KCl and PE and inhibited the maximum relaxations by ACh. In SHR+H and SHR groups, the vasodilation induced by ACh was unaffected by N(G)-nitro-L-arginine methylester (L-NAME), whereas in WKY group, the relaxation to ACh was attenuated by L-NAME. CaCl2-induced contraction in depolarized rings in SHR+H group significantly shifted to the left compared with SHR group. In Ca(2+)-free K-H solution, the maximum contractions induced by PE and caffeine were increased in SHR+H group compared to those in WKY+H group; the PE- and caffeine-induced contractions were also enhanced in SHR group versus WKY group; the maximum contraction induced by PE was significantly increased in SHR+H group versus SHR group. These findings suggest that acute ischemia/hypoxia aggravates mesenteric artery dysfunction in SHR. The mechanism may be related to the decreased NO generation and increased sarcoplasmic reticulum Ca(2+) release.
