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Blockade of AT₁ receptor partially restores vasoreactivity, NOS expression, and superoxide levels in cerebral and carotid arteries of hindlimb unweighting rats

¹Department of Cardiology, Xijing Hospital and ²Department of Aerospace Physiology, Key Laboratory of Aerospace Medicine of Ministry of Education, Fourth Military Medical University, Xi'an; ³Institute of Geriatric Cardiology, PLA General Hospital, Beijing; and ⁴Department of Respiratory Diseases, Xijing Hospital, Fourth Military Medical University, Xi'an, China

Submitted 4 December 2007 ; accepted in final form 5 November 2008

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 KCl/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.

angiotensin II; endothelium-dependent relaxation; nitric oxide synthase; oxidative stress