On the mechanism of catecholamine-induced hyperpolarization of skeletal muscle cells

Naunyn Schmiedebergs Arch Pharmacol. 1985 Mar;329(1):18-23. doi: 10.1007/BF00695186.

Abstract

Catecholamines (noradrenaline, adrenaline and isoprenaline) were tested for their effect on the resting membrane potential of mouse skeletal muscle cells. In freshly isolated muscles incubated in the normal solution containing 5 mol . l-1, catecholamines increased the resting membrane potential (RMP) by 3-5 mV. In Na+-loaded muscles incubated in a K+-free solution, however, catecholamines increased the RMP by 13-16 mV; consequent application of K+ to these muscles did not hyperpolarize the membrane further. A significant decrease of input membrane resistance was observed during the noradrenaline-induced hyperpolarization. This indicates that the passive membrane permeability for K+ ions was apparently increased. Noradrenaline-induced hyperpolarization requires the presence of calcium ions in the incubation solution. We therefore assume that catecholamines hyperpolarize the membrane by Ca2+-dependent K+-channels activation. The action of catecholamines on the resting membrane potential of skeletal muscle exhibits a 50% nonspecific effect as far as the adrenergic receptor is concerned, and the rest may be blocked by adrenergic blocking agents.

MeSH terms

  • Animals
  • Catecholamines / pharmacology*
  • Epinephrine / pharmacology
  • Female
  • In Vitro Techniques
  • Ion Channels / drug effects
  • Isoproterenol / pharmacology
  • Membrane Potentials / drug effects
  • Mice
  • Muscles / drug effects*
  • Norepinephrine / pharmacology
  • Potassium / metabolism
  • Sodium / metabolism
  • Sodium-Potassium-Exchanging ATPase / antagonists & inhibitors
  • Sympatholytics / pharmacology

Substances

  • Catecholamines
  • Ion Channels
  • Sympatholytics
  • Sodium
  • Sodium-Potassium-Exchanging ATPase
  • Isoproterenol
  • Potassium
  • Norepinephrine
  • Epinephrine