Isoprenaline-stimulated differential adrenergic response of K+ channels in skeletal muscle under hypokalaemic conditions.

The mechanism underlying the hyperpolarization induced by isoprenaline in mouse lumbrical muscle fibres was studied using cell-attached patch and intracellular membrane potential ( V(m)) recordings. Sarcolemmal inwardly rectifying K(+) channels (K(IR): 45 pS) and Ca(2+)-activated K(+) channels (BK: 181 pS) were identified. Exposure to isoprenaline closed K(IR) channels and increased BK channel activity. This increase was observed as a shift from 50 to -40 mV in the voltage dependence of channel activation. Isoprenaline prevented hysteresis of V(m) when the extracellular [K(+)] fell below 3.8 mM. This hysteresis was due to the properties of the K(IR). The effects of chloride transport and isoprenaline on V(m) did not interact purely competitively, but isoprenaline could prevent the depolarization induced by hyperosmotic media equally as well as bumetanide, which inhibits the Na(+)/K(+)/2Cl(-) cotransporter. In lumbrical muscle this leads to hyperpolarization, but this might vary among muscles. The switch from K(IR) to BK as the component of total K(+) conductance was due to isoprenaline.