| Autor: |
Ran Zhang, Yun-Gang Bai, Le-Jian Lin, Jun-Xiang Bao, Yu-Yang Zhang, Hao Tang, Jiu-Hua Cheng, Guo-Liang Jia, Xin-Ling Ren, Jin Ma |
| Předmět: |
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| Zdroj: |
Journal of Applied Physiology; Jan2009, Vol. 106 Issue 1, p251-258, 8p, 1 Black and White Photograph, 2 Charts, 3 Graphs |
| Abstrakt: |
Previous studies have demonstrated activation of the local renin-angiotensin system in hindlimb unweighting (HU) rat vasculature. The present study intended to identify the effects of blockade of angiotensin II (ANG II) type 1 (AT1) receptors with losartan on vascular reactivity, nitric oxide synthase (NOS) expression, and superoxide anion (O2.-) levels in 3-wk HU rat cerebral and carotid arteries. Three weeks later, vasoconstriction, vasodilatation, endothelial NOS (eNOS) and inducible NOS (iNOS) protein, as well as O2.- levels in rat cerebral and carotid arteries were examined. We found that HU enhanced maximal response to KCl/5-hydroxytryptamine (P < 0.01) in basilar arteries and KCI/phenylephrine (P < 0.05) in common carotid arteries from HU rats. Acetylcholine induced concentration-dependent vasodilatation in all the artery rings, but with significantly smaller amplitude in basilar (P < 0.01) and common carotid (P < 0.05) arteries from HU rats than those from control rats. Chronic treatment with losartan partially restored response to vasoconstrictors and acetylcholine-induced vasodilatation in basilar (P < 0.01) and common carotid (P < 0.05) arteries from losartan-treated HU rats. Furthermore, iNOS content in cerebral arteries and eNOS/iNOS content in carotid arteries were significantly (P < 0.01) increased in HU rats. Meanwhile, HU increased O2.- levels in all the layers of these arteries. However, losartan restored NOS content and O2.- levels toward normal. These results suggested that the HU-induced enhancement of vasoconstriction and reduction in endothelium-dependent relaxation involved alterations in O2.- and NOS content through an ANG II/AT1 receptor signaling pathway. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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