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Veratridine Induces Vasorelaxation in Mouse Cecocolic Mesenteric Arteries.


ABSTRACT: The vegetal alkaloid toxin veratridine (VTD) is a selective voltage-gated Na+ (NaV) channel activator, widely used as a pharmacological tool in vascular physiology. We have previously shown that NaV channels, expressed in arteries, contribute to vascular tone in mouse mesenteric arteries (MAs). Here, we aimed to better characterize the mechanisms of action of VTD using mouse cecocolic arteries (CAs), a model of resistance artery. Using wire myography, we found that VTD induced vasorelaxation in mouse CAs. This VTD-induced relaxation was insensitive to prazosin, an α1-adrenergic receptor antagonist, but abolished by atropine, a muscarinic receptor antagonist. Indeed, VTD-vasorelaxant effect was totally inhibited by the NaV channel blocker tetrodot

SUBMITTER: Park J 

PROVIDER: S-EPMC11679225 | biostudies-literature | 2024 Dec

REPOSITORIES: biostudies-literature