Figure 6.
Figure 6. Endogenous PIP2 maintains native BK channel activity. (A) Time course of vascular myocyte BK NPo from an I/O patch. Intervals indicate time after patch excision. Arrowheads, baseline; upward deflections, channel openings. Bath application of 0.5 mM ATP and 0.1 μM okadaic acid (OA) increases NPo ×5.4 times. Subsequent application of PIP2 monoclonal antibodies (1:1,000) drastically reduces NPo. V = 40 mV; Ca2+i = 3 μM. (B) Cotransfection of HEK cells with PI4KαII and cbv1+β1 channel subunits causes a parallel leftward shift in the activation–voltage plot when compared with currents mediated by cbv1+β1 alone; n = 5–7.

Endogenous PIP2 maintains native BK channel activity. (A) Time course of vascular myocyte BK NPo from an I/O patch. Intervals indicate time after patch excision. Arrowheads, baseline; upward deflections, channel openings. Bath application of 0.5 mM ATP and 0.1 μM okadaic acid (OA) increases NPo ×5.4 times. Subsequent application of PIP2 monoclonal antibodies (1:1,000) drastically reduces NPo. V = 40 mV; Ca2+i = 3 μM. (B) Cotransfection of HEK cells with PI4KαII and cbv1+β1 channel subunits causes a parallel leftward shift in the activation–voltage plot when compared with currents mediated by cbv1+β1 alone; n = 5–7.

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