Sensitization-induced sodium influx in airway smooth muscle cells of guinea pigs.

Airway smooth muscle (ASM) preparations isolated from Camm-Hartley male guinea pigs were passively in vitro sensitized using Austen's technique. During this sensitization, cells were frequently penetrated with glass microelectrodes (a resistance of 80-90 M omega) for a period of 120 min. Simultaneously, changes in the isometric force of ASM preparations were also monitored. It was found that: administration of serum (1:10 dilution) from sensitized animals caused a depolarization of ASM cells (-52.3 +/- 0.7 mV), achieving a peak at 4 min, followed by slow sustained hyperpolarization reaching a steady state after 15 min; (Resulting resting membrane potential of ASM cells was -68.8 +/- 0.5mV as compared to membrane potential of controls equal to -60.0 +/- 0.7 mV); in the presence of ouabain (10(-5)M), the development of hyperpolarization of ASM cells was completely inhibited; replacement of Na+ with choline chloride or lithium chloride partially inhibited the development of depolarization of ASM cells; in the presence of specific sodium entry blocker, amiloride the sensitization-caused depolarization was abolished; the presence of choline chloride, lithium chloride or amiloride in the experimental medium completely inhibited the contractile response of sensitized tissues to a specific antigen; response of ASM preparations to a specific antigen was absent during depolarization of ASM cells, but was always present during their hyperpolarization. It is concluded that in vitro passive sensitization leads to the interaction of serum specific antibodies with the membrane of airway smooth muscle cells so that permeability of membrane for Na+ is increased (transient depolarization) followed by the activation of electrogenic Na+-pump (sustained hyperpolarization). These events seem to determine the contractile response of sensitized ASM cells to a specific antigen.