BK channels are not involved in the ryanodine‐induced vasoconstriction of the spiral modiolar artery

We investigated whether ryanodine‐sensitive Ca 2+ ‐sparks activate BK channels to lower smooth muscle global Ca 2+ and cause vasodilation in the spiral modiolar artery (SMA). Ca 2+ ‐sparks in the smooth muscle cells of the SMA were abolished by ryanodine at pressures of 40 and 60 cmH 2 O. At 40 cmH 2 O, ryanodine, but not tetracaine, abolished Ca 2+ ‐waves, increased global Ca 2+ and constricted SMA. Iberiotoxin, a BK channel inhibitor, had no effect on either global Ca 2+ or vascular diameter. However, iberiotoxin increased global Ca 2+ and caused a vasoconstriction in the presence of apamin, an inhibitor of SK channels. In contrast to effects at 40 cmH 2 O, ryanodine did not constrict the SMA at 60 cmH 2 O. The pressure‐dependence of the ryanodine‐induced vasoconstriction was consistent with the pressure‐dependence of the Ca 2+ ‐sensitivity, which was greater at 40 than at 60 cmH 2 O. Enhancement of the Ca 2+ ‐sensitivity with 1 nM endothelin‐1 enabled ryanodine‐induced vasoconstriction at 60 cmH 2 O. These results suggest that BK channels are present but not activated by Ca 2+ ‐sparks in the SMA. Instead, regulation of global Ca 2+ and vascular diameter by BK channels is modulated by SK channels. Ryanodine‐induced vasoconstriction is regulated by the Ca 2+ sensitivity and may be caused by store‐dependent mechanisms. Supported by NIH‐R01‐DC04280.