- 期刊
Reduction of Superior Mesenteric Hemodynamic Responsiveness to [Sar^1, Thr^8]-Angiotensin Ⅱ and Bradykinin, But Not Sodium Nitroprusside, in the Presence of Homocysteine Infusion
並列摘要
Hyperhomocsteinemia (HHcy) has been shown to be an independent risk factor for cardiovascu1ar diseases, superior mesenteric thrombosis and inflammatory bowel disease. Superior mesenteric artery (SMA) supplies the intestine and reduced SMA blood f1ow results in intestinal ischemia. Although in vitro studies have shown that endothelium-dependent vasorelaxation of SMA is reduced in the presence of homocysteine incubation, it is not confirmed with in vivo studies. In this work, we evaluated responsiveness of SMA to endothelium-dependent or -independent vasodilators and a vasoconstrictor in the absence and presence of acute HHcy in vivo to clarify effect of HHcy on superior mesenteric vascular function. Sodium nitroprusside (SNP), bradykinin (BK), and [Sar 1, Thr 8] angiotensin Ⅱ [Sar 1, Thr 8] -ANG Ⅱ) were intravenously administrated in sequence in male Sprague-Dawley rats with or without D, L-homocysteine infusion (6 mg/kg/min) through femoral vein. Agonists-induced changes in carotid artery blood pressure, superior mesenteric blood flow and vascular resistance were measured in the present studs. We found that acute HHcy infusion had little effects on SNP-induced hemodynamic changes; however, BK-induced changes in blood pressure, blood flow and vascular resistance were significantly reduced in the presence of HHcy infusion. Additionally, HHcy also markedly decreased [Sar 1, Thr 8] -ANG Ⅱ-induced superior mesenteric hemodynamic changes. These results demonstrated that responsiveness of SMA to vasoconstrictor, endothelium-dependent, but not endothelium-independent vasodilator, was inhibited in the presence of Hcy infusion. This HHcy-associated vascular hyporesponsiveness to vasoconstrictors and endothelium-dependent vasodilators may partially contribute to circulators dysfunctions.
參考文獻
延伸閱讀
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