Calcium-mobilizing and electrophysiological effects of bradykinin on cortical astrocyte subtypes in culture.

The possible consequences of activating bradykinin (Bk) receptors on identified astrocyte subtypes derived from rat cortex have been investigated in terms of: 1) mobilization of intracellular Ca2+; and 2) electrophysiological response. Bk induced a rapid, transient rise in intracellular Ca2+ in 63% of cortical type-1-like astrocytes and 44% of type-2 astrocytes tested. Experiments involving Ca(2+)-free conditions suggested that the release occurred largely from internal stores in both astrocyte subtypes. Bk receptor activation resulted in an inward current in approximately 10% of each astrocyte subtype tested using the whole-cell patch clamp technique. The use of perforated patch recording confirmed a similar population of cells responsive to Bk. The Bk-induced current was associated with a decrease in membrane conductance. The reversal potential was close to the K+ equilibrium potential, consistent with the closure of K+ channels. The current demonstrated similar EC50 values and Hill coefficients and also a marked degree of desensitization for both astrocyte subtypes. Recordings from type-1-like astrocytes indicated that the receptor mediating the electrophysiological response was of the B2 subtype. The data were consistent with the functional translation of Bk receptor occupation to physiological responses in distinct sub-populations of cortical type-1-like and type-2 astrocytes.