Aim:To test the possible involvement of TRPC3 in agonist-induced relaxationand flow-induced vasodilation in rat small mesenteric arteries.Methods:MaleSprague-Dawley rats were used in the present study.After 72 h-treatment ofantisense oligo via tail vein injection,isometric tension and isobaric diametermeasurement were carried out with isolated mesenteric artery segments by usingeither a Pressure Myograph or a Multi Myograph system.Endothelial [Ca~(2+)]_ichanges were measured with a MetaFluor imaging system in response to flow orto 30 nmol/L bradykinin.Results:Immunohistochemical study showed that the72 h-treatment of antisense oligo via tail vein injection markedly decreased theTRPC3 expression in mesenteric arteries,indicating the effectiveness of theantisense oligo.Isometric tension and isobaric diameter measurement showedthat,although the antisense oligo treatment did not affect histamine-,ATP-,andCPA-induced relaxation,it did reduce the magnitude of flow-induced vasodilationby approximately 13% and decreased bradykinin-induced vascular relaxation withits EC_(50) value raised by nearly 3-fold.Endothelial [Ca~(2+)]_i measurement revealedthat treatment of the arteries with antisense oligos significantly attenuated themagnitude of endothelial [Ca~(2+)]_i rise in response to flow and to 30 nmol/L bradykinin.Conclusion:The results suggest that TRPC3 is involved in flow-and bradykinin-induced vasodilation in rat small mesenteric arteries probably by mediating theCa~(2+) influx into endothelial cells. Aim: To test the possible involvement of TRPC3 in agonist-induced relaxation and flow-induced vasodilation in rat small mesenteric arteries. Methods: Male Sprague-Dawley rats were used in the present study. After 72 h-treatment ofantisense oligo via tail vein injection, isometric tension and isobaric diametermeasurement were carried out with isolated mesenteric artery segments by usingeither a Pressure Myograph or a Multi Myograph system. Endothelial [Ca ~ (2 +)] _ ichanges were measured with a MetaFluor imaging system in response to flow orto 30 nmol / L bradykinin . Results: Immunohistochemical study showed that the 72 h-treatment of antisense oligo via tail vein injection markedly decreased the TRPC3 expression in mesenteric arteries, indicating the effectiveness of theantisense oligo. Isometric tension and isobaric diameter measurement showedt, although the antisense oligo treatment did not affect histamine -, ATP-, andCPA-induced relaxation, it did reduce the magnitude of flow-induced vasodilationby appr Endothelial [Ca ~ (2 +)] _i measurement revealed that treatment of the arteries with antisense oligos significantly attenuated the magnity of endothelial [Ca ~ (2 +)] _i rise in response to flow and to 30 nmol / L bradykinin.Conclusion: The results suggest that TRPC3 is involved in flow-and bradykinin-induced vasodilation in rat small mesenteric arteries probably by mediating the Ca ~ (2+) influx into endothelial cells.