Hydrostatic pressure modifies the action of octanol and atropine on frog endplate conductance

1. The effects of octanol, ethanol and atropine were examined on the time course of decay (t_D) of miniature endplate currents (m.e.p.cs) in the frog neuromuscular junction at normal and high pressure.
2. Octanol (25-100 µM) decreased reversibly the t_D of m.e.p.cs in a dose-dependent manner, 100 µM reducing t_D to 0.39 of the control value. Higher concentrations (200-500 µM) additionally depressed the amplitude of m.e.p.cs.
3. Hydrostatic pressure (3.19 and 5.25 MPa) reduced the t_D of octanol (25-100 µM)-shortened m.e.p.cs. Thus 3.19 MPa and 5.25 MPa reduced the t_D in the presence of 100 µM octanol to 0.75 and 0.78 of the octanol treated values. This effect was not completely reversed on decompression. The m.e.p.c. amplitude is reversibly decreased by pressure in the presence of octanol.
4. Hydrostatic pressure (3.19-15.55 MPa) did not modify the effect of ethanol on t_D. At 10.40 and 15.55 MPa the t_D was increased equally in the absence or presence of ethanol.
5. Atropine (60 µM) reduced the t_D and amplitude of m.e.p.cs to 0.33 and 0.63 of the control values. These effects were completely reversible. Hydrostatic pressure (3.19 and 5.25 MPa) reduced the t_D of atropine-shortened m.e.p.cs to 0.82 and 0.77 of the atropine-treated values respectively. This effect was not completely reversed on decompression. Hydrostatic pressure also reversibly depressed the amplitude of atropine-treated m.e.p.cs.
6. The implications of these drug-hydrostatic pressure interactions are discussed.