The effect of cortisol on the excitability of the rat muscle fibre membrane and neuromuscular transmission
Jazyk angličtina Země Česko Médium print
Typ dokumentu časopisecké články
PubMed
230528
Knihovny.cz E-zdroje
- MeSH
- acetylcholin farmakologie MeSH
- akční potenciály účinky léků MeSH
- bránice metabolismus fyziologie MeSH
- dinitrofenoly farmakologie MeSH
- elektrofyziologie MeSH
- hydrokortison farmakologie MeSH
- krysa rodu Rattus MeSH
- membránové potenciály účinky léků MeSH
- nervosvalové spojení fyziologie MeSH
- nervový přenos účinky léků MeSH
- prednisolon farmakologie MeSH
- spotřeba kyslíku účinky léků MeSH
- svaly metabolismus fyziologie MeSH
- techniky in vitro MeSH
- tetrodotoxin farmakologie MeSH
- zvířata MeSH
- Check Tag
- krysa rodu Rattus MeSH
- ženské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- Názvy látek
- acetylcholin MeSH
- dinitrofenoly MeSH
- hydrokortison MeSH
- prednisolon 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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