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.
journal_name
Vascul Pharmacoljournal_title
Vascular pharmacologyauthors
de Oliveira LM,de Oliveira TS,da Costa RM,de Souza Gil E,Costa EA,Passaglia Rde C,Filgueira FP,Ghedini PCdoi
10.1016/j.vph.2015.10.010subject
Has Abstractpub_date
2016-06-01 00:00:00pages
69-74eissn
1537-1891issn
1879-3649pii
S1537-1891(15)30035-5journal_volume
81pub_type
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