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

The effects of octanol, ethanol and atropine were examined on the time course of decay (tau D) of miniature endplate currents (m.e.p.cs) in the frog neuromuscular junction at normal and high pressure. Octanol (25-100 microM) decreased reversibly the tau D of m.e.p.cs in a dose-dependent manner, 100 microM reducing tau D to 0.39 of the control value. Higher concentrations (200-500 microM) additionally depressed the amplitude of m.e.p.cs. Hydrostatic pressure (3.19 and 5.25 MPa) reduced the tau D of octanol (25-100 microM)-shortened m.e.p.cs. Thus 3.19 MPa and 5.25 MPa reduced the tau D in the presence of 100 microM 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. Hydrostatic pressure (3.19-15.55 MPa) did not modify the effect of ethanol on tau D. At 10.40 and 15.55 MPa the tau D was increased equally in the absence or presence of ethanol. Atropine (60 microM) reduced the tau 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 tau 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. The implications of these drug-hydrostatic pressure interactions are discussed.