Ca v 3.2 T‐type Ca++ channels trigger the endothelium‐dependent vasodilator signals activated by electrical stimulation.

Electrical stimulation induces vasodilator responses that spread along the vessel length without decay. We studied the transduction signals involved in the electrically induced conducted vasodilation. Mouse cremasteric arterioles were stimulated electrically (30Hz, 2ms, 30V) for 10s and the vasomotor response was evaluated at the stimulation site (local) and at 500, 1000 and 2000μm upstream. Electrical stimulation evoked local constriction and a conducted dilation. Perfusion of 10μM BAPTA‐AM for 10 min enhanced and prolonged the local constriction. Moreover, after endothelial cell BAPTA loading, the conducted dilation was delayed, smaller, and slower than control. Topical application of 10μM Ni ++ or 100μM amiloride elicited vasoconstriction and blocked the electrically induced vasodilation, but not the propagation of the response, which suggests the activation of a Ca v 3.2‐dependent vasodilator signal. Consistent with this idea, a similar result was found in Ca v 3.2 knockout mice. In addition, the resting arteriolar tone and blood pressure were higher in Ca v 3.2 knockout mice than in controls. These results indicate that an endothelial cell Ca ++ influx via activation of Ca v 3.2 channels triggers the vasodilator response induced by electrical stimulation. Deletion of Ca v 3.2 demonstrates that these channels are key in the vascular control of blood pressure. Grants: NIH #HL53318, AHA #0325730U.