Effect of iron on vasoconstriction in the isolated rat aorta.
- Author:
Wei KUANG
1
;
Ying-Ying CHEN
;
Yue-Liang SHEN
;
Qiang XIA
Author Information
1. Department of Physiology, Zhejiang University School of Medicine, Hangzhou 310031.
- Publication Type:Journal Article
- MeSH:
Animals;
Aorta, Thoracic;
physiology;
Calcium;
metabolism;
Calcium Channels, L-Type;
metabolism;
Ferric Compounds;
pharmacology;
Glutathione;
metabolism;
In Vitro Techniques;
Iron;
pharmacology;
Male;
Muscle, Smooth, Vascular;
drug effects;
physiology;
Quaternary Ammonium Compounds;
pharmacology;
Rats;
Rats, Sprague-Dawley;
Reactive Oxygen Species;
metabolism;
Vasoconstriction;
drug effects;
physiology
- From:
Acta Physiologica Sinica
2003;55(3):273-277
- CountryChina
- Language:Chinese
-
Abstract:
The present study was to examine the effect of iron on isolated rat aortic rings, and to elucidate the underlying mechanism. The thoracic aortic rings without endothelium of male Sprague-Dawley rats were mounted on a bath system. Isometric contractions of aortic rings were measured. The results obtained are as follows. (1) Ferric ammonium citrate (FAC) (100 micromol/L) caused a phasic response with an initial transient contraction followed by a relaxation in thoracic aortic ring. The maximal contractile amplitude was 24.02+/-2.37% of the maximal contraction induced by KCl, the duration of phasic contraction lasted for about 20 min. (2) In high Ca(2+) Krebs-Henseleit (K-H) solution (twice of the normal concentration), the contractile amplitude induced by FAC was enhanced. After the aortic rings were incubated with nifedipine for 15 min to block the L-type Ca(2+) channel, the iron-induced contraction was attenuated. (3) In Ca(2+)-free K-H solution, addition of FAC caused a strong and sustained contraction in the presence of PDBu. (4) Pretreatment of FAC for 30 min decreased the KCl-induced contraction and also caused a significant reduction in the contractile response to phenylephrine (PE). Pretreatment of the arteries with DMSO, catalase or glutathione before FAC exposure prevented the decrease in contraction responses to PE (P<0.05). It is therefore concluded that iron causes phasic contraction of vascular smooth muscle, in which both extracellular Ca(2+) entry through L-type Ca(2+) channel and increase in Ca(2+) sensitivity of smooth muscle cells are involved. Exposure to iron causes inhibitory effects on KCl- or PE-induced contractions in isolated thoracic arteries. Reactive oxygen species and glutathione may be involved in iron-induced contraction dysfunction.
