The effect of cortisol on the excitability of the rat muscle fibre membrane and neuromuscular transmission
Language English Country Czech Republic Media print
Document type Journal Article
PubMed
230528
Knihovny.cz E-resources
- MeSH
- Acetylcholine pharmacology MeSH
- Action Potentials drug effects MeSH
- Diaphragm metabolism physiology MeSH
- Dinitrophenols pharmacology MeSH
- Electrophysiology MeSH
- Hydrocortisone pharmacology MeSH
- Rats MeSH
- Membrane Potentials drug effects MeSH
- Neuromuscular Junction physiology MeSH
- Synaptic Transmission drug effects MeSH
- Prednisolone pharmacology MeSH
- Oxygen Consumption drug effects MeSH
- Muscles metabolism physiology MeSH
- In Vitro Techniques MeSH
- Tetrodotoxin pharmacology MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Female MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Names of Substances
- Acetylcholine MeSH
- Dinitrophenols MeSH
- Hydrocortisone MeSH
- Prednisolone MeSH
- Tetrodotoxin MeSH
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.
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