Please use this identifier to cite or link to this item: http://hdl.handle.net/20.500.12779/4814
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dc.contributor.authorFusi, Fabioen_us
dc.contributor.authorSaponara, Simonaen_us
dc.contributor.authorFrosini, Mariaen_us
dc.contributor.authorGorelli, Ben_us
dc.contributor.authorSgaragli, GIAN PIETROen_us
dc.date.accessioned2021-03-30T15:44:53Z-
dc.date.available2021-03-30T15:44:53Z-
dc.date.issued2003-
dc.identifier.issn0028-1298en_US
dc.identifier.urihttp://hdl.handle.net/20.500.12779/4814-
dc.description35219en_US
dc.description.abstractThe effects of myricetin (3,3',4',5,5',7-hesahydroxyflavone), a natural flavonoid found in edible plants, were studied on vascular smooth muscle L-type Ca(2+) channels by comparing its mechanical, radioligand binding, and electrophysiological properties to those of the Ca(2+) channel agonist (S)-(-)-Bay K 8644. In rat aorta rings, both myricetin and (S)-(-)-Bay K 8644 induced contractile responses, which were dependent upon prior exposure to K(+). At 15 mM K(+) (K15) the pEC(50) values for myricetin and (S)-(-)-Bay K 8644 were 4.43+/-0.03 and 7.92+/-0.13, respectively. Furthermore, the maximum tension response to myricetin was not significantly different from that elicited by either (S)-(-)-Bay K 8644 or K60. The Ca(2+) channel blockers nifedipine, verapamil and diltiazem antagonised and fully reverted myricetin-, (S)-(-)-Bay K 8644- as well as K60-induced contractions. Both myricetin and (S)-(-)-Bay K 8644 potentiated rat aorta ring responses to K(+), shifting the K(+) concentration-response curve to the left. (S)-(-)-Bay K 8644, but not myricetin, inhibited in a concentration-dependent manner (+)-[(3)H]PN200-110 binding in porcine aortic membranes. Electrophysiological recordings from single rat tail artery myocytes, under amphotericin B-perforated as well as conventional methods, showed that both myricetin and (S)-(-)-Bay K 8644 increased L-type Ba(2+) current (I(Ba(L))) and shifted the maximum of the current-voltage relationship by 10 mV in the hyperpolarising direction, without, however, modifying the threshold potential. Furthermore, (S)-(-)-Bay K 8644 accelerated both activation and inactivation kinetics of I(Ba(L)) while myricetin slowed down the activation kinetics. Finally, both (S)-(-)-Bay K 8644 and myricetin slowed down deactivation kinetics of I(Ba(L)). These results suggest that myricetin induces vasoconstriction by activating L-type Ca(2+) channel with similar efficacy but a site of action different to that of (S)-(-)-Bay K 8644.en_US
dc.language.isoenen_US
dc.relationNoneen_US
dc.relation.ispartofNAUNYN-SCHMIEDEBERG'S ARCHIVES OF PHARMACOLOGYen_US
dc.titleL-type Ca2+ channels activation and contraction elicited by myricetin on vascular smooth muscles.en_US
dc.typeArticleen_US
dc.identifier.doi10.1007/s00210-003-0836-yen_US
dc.identifier.pmid14618297en_US
dc.identifier.scopus2-s2.0-0347361480en_US
dc.identifier.isiWOS:000187291900005en_US
dc.relation.volume368en_US
dc.relation.issue6en_US
dc.description.firstpage470en_US
dc.description.lastpage478en_US
dc.description.thirdmissionNot applicableen_US
item.cerifentitytypePublications-
item.grantfulltextnone-
item.languageiso639-1en-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.openairetypeArticle-
item.fulltextNo Fulltext-
crisitem.author.orcid0000-0002-5737-8309-
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