Muscarinic receptor–mediated, global Ca2+ signals are similar in native endothelial cells of hypertensive and normotensive mice.20 However, local signals arising from TRPV4 (transient receptor potential vanilloid 4)-mediated Ca2+ influx are reduced.20 This latter observation demonstrates that disruption of local Ca2+ signaling circuits, rather than global increases in Ca2+, may contribute to endothelial dysfunction in hypertension.20 The gene discussed is TRPV4; the disease is hypertensive disorder.