A novel mechanism of vascular relaxation induced by sodium nitroprusside in the isolated rat aorta

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• 作者：Daniella Bonaventura ; Claure N. Lunardi ; Gerson J. Rodrigues ; Má ; rio A. Neto ; Lusiane M. Bendhack
• 关键词：Sodium nitroprusside ; Nitric oxide ; NO-synthase ; Endothelium ; Vasorelaxation ; Ca²⁺ transient
• 刊名：Nitric Oxide
• 出版年：2008
• 期刊代码：181_10898603
• 类别：bio
• 出版时间：June 2008
• 卷：18
• 期：4
• 页码：287-295
• 文件大小：857 K

摘要

Sodium nitroprusside (SNP) is an endothelium-independent relaxant agent and its effect is attributed to its direct action on the vascular smooth muscle (VSM). Endothelium modulates the vascular tone through the release of vasoactive agents, such as NO. The aim of this study was to investigate the contribution of the endothelium on SNP vasorelaxation, NO release and Ca²⁺ mobilization. Vascular reactivity experiments showed that endothelium potentiates the SNP-relaxation in rat aortic rings and this effect was abolished by l-NAME. SNP-relaxation in intact endothelium aorta was inhibited by NOS inhibitors for the constitutive isoforms (cNOS). Furthermore, endogenous NO is involved on the SNP-effect and this endogenous NO is released by cNOS. Moreover, Ca²⁺ mobilization study shows that l-NAME inhibited the reduction of Ca²⁺-concentration in VSM cells and reduced the increase in Ca²⁺-concentration in endothelial cells induced by SNP. This enhancement in Ca²⁺-concentration in the endothelial cells is due to a voltage-dependent Ca²⁺ channels activation. The present findings indicate that the relaxation and [Ca²⁺]_i decrease induced by SNP in VSM cells is potentiated by endothelial production of NO by cNOS-activation in rat aorta.