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Activating TRPV4 with endogenous and synthetic agonists inhibited ANGII-mediated G-protein associated second messenger accumulation, AT1R receptor phosphorylation and β-arrestin recruitment. We also noted that TRPV4 inhibits AT1R phosphorylation by activating the calcium-activated phosphatase calcineurin in a Ca2+/calmodulin dependent manner, preventing β-arrestin recruitment and receptor internalization. These findings suggest that when TRP channels and GPCRs are co-expressed in the same tissues, many of these channels can inhibit GPCR de
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