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The Vasorelaxant Effect of Gallic Acid Involves Endothelium-Dependent and -Independent Mechanisms

The Vasorelaxant Effect of Gallic Acid Involves Endothelium-Dependent and -Independent Mechanisms

Lais Moraes de Oliveira, Thiago Sardinha de Oliveira, Rafael Menezes da Costa, Eric de Souza Gil, Elson Alves Costa, Rita de Cassia Aleixo Tostes Passaglia, Fernando Paranaíba Filgueira, Paulo César Ghedini

Vascul Pharmacol. 2016 Jun;81:69-74.

PMID: 26643780

Abstract:

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 (0.4-10mM) 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 10mM) 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.

Chemicals Related in the Paper:

Catalog Number	Product Name	Structure	CAS Number	Price
IAR42415684	InSolution PP2			Price

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