Abstract:NO controls the activity of canonical transient receptor potential channel (TRPC) in endothelial cells. Our group already provided evidences that reduced NO bioavailability was directly linked to increased basal cytosolic Ca2+ in a cellular model of endothelial dysfunction. The aim of this study was to evaluate the role of TRPC3 channels in Ca2+ homeostasis of aortic porcine endothelial cells (PAEC). In PAEC at P1, producing NO, specific inhibition of TRPC3 by Pyr3 induced a concentration‐dependent decrease in… Show more
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