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. 2019 Sep 2;14:1579–1587. doi: 10.2147/CIA.S220283

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© 2019 Huang et al.

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Role of TRPV4-K_Ca2.3 signaling in acetylcholine (ACh)-induced, endothelium-derived hyperpolarizing factor (EDHF)-mediated relaxation in rat aortic arteries. Representative traces (A, C) and summary data (B, D) for ACh-induced, EDHF-mediated relaxation and the effect of transient receptor potential vanilloid 4 (TRPV4) or small-conductance calcium-activated potassium channel (K_Ca2.3) inhibition. The EDHF response was induced by 10 μmol/L of ACh (n=10) or 300 nmol/L of the TRPV4 activator GSK1016790A (n=3) in the presence of 7 μmol/L of indomethacin and 300 μmol/L of NG-nitro-L-arginine (n=5). Preincubation with 20 µmol/L of the TRPV4 inhibitor RN1734 (n=4) or with 200 nmol/L of the K_Ca2.3 inhibitor apamin (n=4) decreased the ACh-induced, EDHF-mediated relaxation in the presence of indomethacin and L-NNA. Values are the mean ± SEM. **P<0.01, ***P<0.001 vs. Ctrl; ^##P<0.01 vs. L-NNA + Indo. Phe, indicates phenylephrine; Ctrl, control; Indo, indomethacin; L-NNA, NG-nitro-L-arginine; Apa, apamin; and GSK, GSK1016790A.