Interleukin-2 induced endothelium-dependent relaxation of rat thoracic aorta.
- Author:
Chun-Mei CAO
1
;
Song YE
;
Hu YU
;
Qing-Sheng XU
;
Zhi-Guo YE
;
Yue-Liang SHEN
;
Yuan LU
;
Qiang XIA
Author Information
1. Department of Physiology, Zhejiang University School of Medicine, Hangzhou 310031.
- Publication Type:Journal Article
- MeSH:
Animals;
Aorta, Thoracic;
drug effects;
physiology;
Endothelium, Vascular;
drug effects;
Endothelium-Dependent Relaxing Factors;
pharmacology;
Guanylate Cyclase;
metabolism;
In Vitro Techniques;
Interleukin-2;
pharmacology;
Male;
NG-Nitroarginine Methyl Ester;
pharmacology;
Nitric Oxide;
metabolism;
Prostaglandin-Endoperoxide Synthases;
metabolism;
Rats;
Rats, Sprague-Dawley;
Signal Transduction;
drug effects;
Vasodilation;
drug effects;
Vasodilator Agents;
pharmacology
- From:
Acta Physiologica Sinica
2003;55(1):19-23
- CountryChina
- Language:Chinese
-
Abstract:
Interleukin-2 (IL-2) therapy often results in potentially life-threatening side effects including hypotension. However, the mechanism has not been completely elucidated. In order to determine whether IL-2 modifies vascular tone, we investigated the effect of IL-2 on rat thoracic aorta rings and the underlying mechanisms. Effects of IL-2 on the contraction of high KCl and phenylephrine (PE) preconstricted rat thoracic aorta with or without endothelium were determined by organ bath technique. To explore the mechanism, nitric oxide synthase inhibitor L-N(G)-nitroarginine methyl ester (L-NAME), guanylyl cyclase inhibitor methylene blue, and cyclooxygenase inhibitor indomethacin were used. IL-2 (10-1000 U/ml) caused concentration-dependent relaxation of aorta rings preconstricted with PE (10 micromol/L) in endothelium-intact rings, but had no effect on KCl (120 mmol/L) preconstricted rings. Removal of the endothelium, or pretreatment with L-NAME (0.1 mmol/L) or methylene blue (10 micromol/L) or indomethacin (10 micromol/L), inhibited the relaxation of IL-2. The results indicate that the relaxation by IL-2 in rat aorta ring is endothelium-dependent and is possibly mediated by the NO-guanylyl cyclase pathway and cyclooxygenase-dependent pathway.
