Supplementary Material for: Role of TRPC1 and TRPC3 Channels in Contraction and Relaxation of Mouse Thoracic Aorta

<b><i>Background/Aims:</i></b> Canonical transient receptor potential (TRPC) channels modulate membrane potential and intracellular Ca²⁺. We examined the role of TRPC1 and TRPC3 channels in vasocontraction and relaxation in mouse aorta. <b><i>Methods:</i></b> Vasocontraction and relaxation of aorta from wild-type (WT), TRPC1 KO and TRPC3 knockout (KO) mice were measured for phenylephrine (Phe) and carbachol (CCh). Intracellular Ca²⁺ was measured in primary aorta endothelial cells (EC) and whole cell K⁺ current in freshly isolated smooth muscle cells (SMC). <b><i>Results and Conclusion:</i></b> TRPC1 KO aorta showed increased vasocontraction to Phe compared to WT and TRPC3 KO aorta due to diminished role of BK_Ca channels. BK_Ca mRNA (aorta) and whole cell current (SMC) were reduced versus WT. Contraction in WT aorta was increased to TRPC1 KO level by BK_Ca channel inhibition. Relaxation to CCh was reduced in TRPC1 KO and TRPC3 KO aortas with concomitant reduction in EC Ca²⁺ response. Pyr3 (TRPC3 blocker) reduced the Ca²⁺ response to CCh in EC from WT, but not TRPC3 KO mice. In summary, TRPC1 attenuates receptor-mediated contraction through activation and/or expression of SMC BK_Ca channels while TRPC3 does not contribute to receptor-mediated constriction. Both TRPC1 and TRPC3 participate in EC Ca²⁺ influx and vasorelaxation of aorta.