The smooth muscle-type β1 subunit potentiates activation by DiBAC4(3) in recombinant BK channels.

Large-conductance Ca(2+)-activated (BK) channels, expressed in a variety of tissues, play a fundamental role in regulating and maintaining arterial tone. We recently demonstrated that the slow voltage indicator DiBAC4(3) does not depend, as initially proposed, on the β 1 or β 4 subunits to activate native arterial smooth muscle BK channels. Using recombinant mslo BK channels, we now show that the β 1 subunit is not essential to this activation but exerts a large potentiating effect. DiBAC4(3) promotes concentration-dependent activation of BK channels and slows deactivation kinetics, changes that are independent of Ca(2+). Kd values for BK channel activation by DiBAC4(3) in 0 mM Ca(2+) are approximately 20 μM (α) and 5 μM (α+β 1), and G-V curves shift up to -40 mV and -110 mV, respectively. β1 to β2 mutations R11A and C18E do not interfere with the potentiating effect of the subunit. Our findings should help refine the role of the β 1 subunit in cardiovascular pharmacology.