Ca2+-sensitive K+ channels in phagocytic cell membranes

In phagocytic cells evidence for properties of Ca2+-sensitive K+-selective channels comes mostly from electrophysiological studies. Macrophages and macrophage-like cells are compared with fibroblasts (L-cells) where the Ca+-dependent K+ conductance is better understood. This model shares a mesenchymal origin and an accessory phagocytic capacity with the professional phagocytes. In macrophages several values of transmembrane potentials have been measured by different groups, using various techniques. Microelectrode measurements have demonstrated a voltage-dependent K+ conductance involved in transition from low to high membrane potentials. Current-voltage relationships in mouse peritoneal exudate cells have revealed a region of negative slope resistance. Slow calcium spikes were found in a subpopulation of cells from human dialysis fluid that appear to be distinct from typical macrophages. Action potentials have been recorded from human monocyte-derived macrophages. Their ionic mechanism has not yet been established. Spontaneous and electrically elicited slow membrane hyperpolarizations have been described in macrophages and macrophage-like cells. Similar activity is well known in L-cells and in both cases it is possible to identify a Ca2+-sensitive K+ conductance as the underlying mechanism. Phagocytosis is a cell function that has been related to membrane hyperpolarization and to slow hyperpolarizing activity. In some cases no changes of electrical activity have been observed during the phagocytic process. Chemotactic factors induce membrane hyperpolarizations in macrophages, but the relation between electrical change and cell motility has not been established. Exocytosis, a is another Ca2+ sensitive cell function that awaits correlation with electrochemical changes. The evidences accumulated to date are compatible with several models for gating and modulation of the voltage-independent K+ conductance by Ca2+. The use of higher resolution techniques, such as patch-clamp, with well defined subpopulations of phagocytic cells may produce the missing link in the transduction of membrane signals into the specifically targeted cell functions.