Delayed rectifying and calcium-activated K+ channels and their significance for action potential repolarization in mouse pancreatic beta-cells.

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Abstract
The contribution of Ca2+-activated and delayed rectifying K+ channels to the voltage-dependent outward current involved in spike repolarization in mouse pancreatic .beta.-cells (Rorsman, P., and G. Trube. 1986, J. Physiol. 374:531-550) was assessed using patch-clamp techniques. A Ca2+-dependent component could be identified by its rapid inactivation and sensitivity to the Ca2+ channel blocker Cd2+. This current showed the same voltage dependence as the voltage-activated (Cd2+-sensitive) Ca2+ currents and contributed 10-20% to the total .beta.-cell delayed outward current. The single-channel events underlying the Ca2+-activated component were investigated in cell-attached patches. Increase of [Ca2+]i invariably induced a dramatic increase in the open state probability of a Ca2+-activated K+ channel. This channel had a single-channel conductance of 70 pS ([K+]o = 5.6 mM). The Ca2+-dependent outward current (constituting > 80% of the total) reflected the activation of an 6 pS ([K+]o = 5.6 mM: [K+]i = 155 mM) K+ channel. This channel was the only type observed to be associated with action potentials in cell-attached patches. It is suggested that in mouse .beta.-cells spike repolarization results mainly from the opening of the 8-pS delayed rectifying K+ channel.

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