The vasorelaxant effect of gallic acid involves endothelium-dependent and -independent mechanisms

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• 作者：Lais Moraes de Oliveira^a ; Thiago Sardinha de Oliveira^a ; Rafael Menezes da Costa^b ; Eric de Souza Gil^c ; Elson Alves Costa^d ; Rita de Cassia Aleixo Tostes Passaglia^b ; Fernando Paranaí ; ba Filgueira^e ; Paulo Cé ; sar Ghedini^a ; ^{pcghedini@gmail.com" class="auth_mail" title="E-mail the corresponding author}
• 关键词：Gallic acid ; Rat thoracic aorta ; Vasorelaxant ; Calcium channel ; Potassium channels ; Nitric oxide
• 刊名：Vascular Pharmacology
• 出版年：2016
• 出版时间：June 2016
• 年：2016
• 卷：81
• 期：Complete
• 页码：69-74
• 全文大小：713 K

文摘

The mechanisms of action involved in the vasorelaxant effect of gallic acid (GA) were examined in the isolated rat thoracic aorta. GA exerted a relaxant effect in the highest concentrations (0.4–10 mM) in both endothelium-intact and endothelium-denuded aortic rings. Pre-incubation with L-NAME, ODQ, calmidazolium, TEA, 4-aminopyridine, and barium chloride significantly reduced the pEC₅₀ values. Moreover, this effect was not modified by indomethacin, wortmannin, PP2, glibenclamide, or paxillin. Pre-incubation of GA (1, 3, and 10 mM) in a Ca^2 +-free Krebs solution attenuated CaCl₂-induced contractions and blocked BAY K8644-induced vascular contractions, but it did not inhibit a contraction induced by the release of Ca^2 + from the sarcoplasmatic reticulum stores. In addition, a Western blot analysis showed that GA induces phosphorylation of eNOS in rat thoracic aorta. These results suggest that GA induces relaxation in rat aortic rings through an endothelium-dependent pathway, resulting in eNOS phosphorylation and opening potassium channels. Additionally, the relaxant effect by an endothelium-independent pathway involves the blockade of the Ca^2 + influx via L-type Ca^2 + channels.