Adrenergic control of Na+-K+-homoeostasis

Acta Med Scand Suppl. 1983;672:111-5. doi: 10.1111/j.0954-6820.1983.tb01622.x.

Abstract

Catecholamines induce hypokalaemia via stimulation of beta-adrenoceptors, primarily in skeletal muscle but also in other tissues. This is the result of increased active Na+-K+-transport, leading to a rise in the intracellular K+/Na+-ratio and hyperpolarisation in muscle cells. These effects are mediated by 3', 5'-cyclic adenosine monophosphate, can be detected down to physiological concentrations of adrenaline and noradrenaline, and are seen both in vitro and in vivo. Catecholamines released from the adrenal medulla as well as sympathetic nerve endings are of importance in clearing K+ from the extracellular water space during K+-loading or exercise. beta 2-adrenoceptor agonists can be used in the treatment of hyperkalaemia, and beta-adrenoceptor blockade may induce hyperkalaemia, in particular during exercise. The effects of catecholamines on the contractile performance of skeletal muscles are partly due to stimulation of the active electrogenic Na+-K+-transport across the sarcolemma.

Publication types

  • Review

MeSH terms

  • Adrenergic beta-Agonists / therapeutic use
  • Adrenergic beta-Antagonists / pharmacology
  • Animals
  • Biological Transport, Active / drug effects
  • Catecholamines / pharmacology*
  • Epinephrine / pharmacology
  • Homeostasis / drug effects*
  • Humans
  • Hyperkalemia / drug therapy
  • Ion Channels / drug effects
  • Membrane Potentials / drug effects
  • Muscles / physiology
  • Norepinephrine / pharmacology
  • Ouabain / pharmacology
  • Physical Exertion / drug effects
  • Potassium / blood
  • Potassium / metabolism*
  • Sodium / metabolism*
  • Sympathectomy

Substances

  • Adrenergic beta-Agonists
  • Adrenergic beta-Antagonists
  • Catecholamines
  • Ion Channels
  • Ouabain
  • Sodium
  • Potassium
  • Norepinephrine
  • Epinephrine