TRPV4 and hypertensive disorder: In isolated mouse mesenteric arteries, activation of smooth muscle α1ARs elicits vasoconstriction for ~2 min followed by a slow dilation induced by increases in endothelial TRPV4-mediated Ca2+ influx and activation of KCa channels, a mechanism that may cease prolonged vascular resistance and hypertension as observed in TRPV4−/− mice [108].