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Hydrostatic pressure modifies the action of octanol and atropine on frog endplate conductance
Author(s) -
Ashford M.L.J.,
Macdonald A.G.,
Wann K.T.
Publication year - 1984
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1984.tb16510.x
Subject(s) - chemistry , atropine , hydrostatic pressure , octanol , conductance , ethanol , chromatography , medicine , biochemistry , partition coefficient , thermodynamics , physics , condensed matter physics
1 The effects of octanol, ethanol and atropine were examined on the time course of decay (τ D ) of miniature endplate currents (m.e.p.cs) in the frog neuromuscular junction at normal and high pressure. 2 Octanol (25–100 μ M ) decreased reversibly the τ D of m.e.p.cs in a dose‐dependent manner, 100 μ M reducing τ D to 0.39 of the control value. Higher concentrations (200–500 μ M ) additionally depressed the amplitude of m.e.p.cs. 3 Hydrostatic pressure (3.19 and 5.25 MPa) reduced the τ D of octanol (25–100 μ M )‐shortened m.e.p.cs. Thus 3.19 MPa and 5.25 MPa reduced the τ D in the presence of 100 μ M 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 τ D . At 10.40 and 15.55 MPa the τ D was increased equally in the absence or presence of ethanol. 5 Atropine (60 μ M ) reduced the τ D and amplitude of m.e.p.cs to 0.33 and 0.63 of the control values. These effects were compeletely reversible. Hydrostatic pressure (3.19 and 5.25 MPa) reduced the τ 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.