The effect of cortisol on the excitability of the rat muscle fibre membrane and neuromuscular transmission.
The present experiments show that cortisol when applied in vitro, exerted two different effects on the electrical excitability of the diaphragm muscle fibre membrane and on the neuromuscular transmission depending on the concentration used. At low concentrations (2.5X10(-6) mol.l-1) it potentiated action potentials, increased resting membrane polarization by 3--4 mV and did not affect neuromuscular transmission. Higher concentrations (10(-2) mol.l-1) suppressed the action potential to a certain extent, depolarized the muscle fibre membrane by 6 mV and reduced the amplitudes of m.e.p.p.s and e.p.p.s as well as those of iontophoretically evoked acetylcholine potentials. It was concluded that the effect of low concentrations of cortisol is primary and is probably due to the enhancement of resting membrane permeability for K+ ions and to the changes in ion channels. Cortisol in high doses increased muscle oxygen consumption, so that its suppressing effect might be due to inhibition of energy metabolism.
D000109:Acetylcholine / Q000494:pharmacology; D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D003964:Diaphragm / Q000378:metabolism / Q000502:physiology; D004140:Dinitrophenols / Q000494:pharmacology; D004594:Electrophysiology; D005260:Female; D006854:Hydrocortisone / Q000494:pharmacology*; D066298:In Vitro Techniques; D008564:Membrane Potentials / Q000187:drug effects; D009132:Muscles / Q000378:metabolism / Q000502:physiology*; D009469:Neuromuscular Junction / Q000502:physiology*; D010101:Oxygen Consumption / Q000187:drug effects; D011239:Prednisolone / Q000494:pharmacology; D051381:Rats; D009435:Synaptic Transmission / Q000187:drug effects*; D013779:Tetrodotoxin / Q000494:pharmacology
D004140:Dinitrophenols; D013779:Tetrodotoxin; D011239:Prednisolone; D000109:Acetylcholine; D006854:Hydrocortisone