Figure 3.

Effects of apamin on the relaxation and hyperpolarization phases of PAR responses

A and B, representative traces showing that apamin (300 nm) pretreatment abolished thrombin (50 U ml⁻¹; A) and trypsin (1 μm; B)-induced relaxation phase and caused development of tone in these phasic muscles. C and D, intracellular microelectrode recordings of transmembrane potentials showing that thrombin (50 U ml⁻¹; C) and trypsin (1 μm; D) induced depolarization and sustained firing of action potentials when the hyperpolarization phase of PAR responses was blocked by apamin (300 nm). E and F, thrombin (50 U ml⁻¹; E) and trypsin (1 μm; F)-induced depolarization were completely abolished by pretreatment of NPPB (10 μm).