The first demonstration that internal calcium is able to regulate potassium flux across membranes was given by Gardos (19) in red blood cells. A more direct approach to this problem was taken by Meech & Strumwasser (51), who observed that a microinjection of calcium was able to hyperpolarize the cell membrane of an Aplysia neuron. This response is accompanied by an increase in membrane conductance, and its reversal potential is a function of the external potassium concentration (49). On the basis of these results, a Ca2+ activated K+ conductance, GK (Ca), was postulated, and Meech (50) suggested that the main role of these channels probably is to link cell metabolism to membrane conductance. Since these seminal observations were made, studies using the patch-clamp (60) and reconstitution techniques (53) have demon strated that intracellular calcium activates several different K+ channels (for reviews see 11, 34, 37, 65). Channel conductance, calcium sensitivity, voltage dependence, and pharmacological properties have been used to distin guish between the different channels of this family. Channel conductance ranges from a few to several hundred picosiemens (pS) consequently, at tempts have been made to group K (Ca) channels according to their con ductance (11, 36). They have been called small potassium (SK; 10, 11) and