Na+,K+-ATPase inhibitors and the adrenergic neuroeffector interaction in the blood vessel wall

J Cardiovasc Pharmacol. 1984:6 Suppl 1:S88-94. doi: 10.1097/00005344-198400061-00016.

Abstract

Augmentation of the constrictor response of blood vessels to sympathetic nerve stimulation caused by inhibitors of Na+,K+-ATPase can be explained by (a) inhibition of neuronal uptake, (b) displacement of stored norepinephrine, (c) facilitation of exocytotic release of the adrenergic transmitter, (d) diminution in intraneuronal deamination, (e) reduction in extraneuronal uptake, (f) facilitation of postjunctional alpha 2-adrenoceptors, (g) inhibition of poststimulation relaxation, and, possibly, (h) prevention of endothelium-dependent relaxation.

Publication types

  • Review

MeSH terms

  • Animals
  • Dinoprost
  • Dogs
  • Endothelium / drug effects
  • Hydroxydopamines / pharmacology
  • In Vitro Techniques
  • Muscle Relaxation / drug effects
  • Muscle, Smooth, Vascular / innervation
  • Muscle, Smooth, Vascular / physiology*
  • Neuroeffector Junction / drug effects
  • Neurons / metabolism
  • Neurotransmitter Agents / physiology*
  • Norepinephrine / metabolism
  • Ouabain / pharmacology
  • Oxidopamine
  • Prostaglandins F / pharmacology
  • Receptors, Adrenergic, alpha / drug effects
  • Sodium-Potassium-Exchanging ATPase / antagonists & inhibitors*
  • Strophanthidin / analogs & derivatives
  • Strophanthidin / pharmacology
  • Sympathectomy, Chemical
  • Sympathetic Nervous System / drug effects*

Substances

  • Hydroxydopamines
  • Neurotransmitter Agents
  • Prostaglandins F
  • Receptors, Adrenergic, alpha
  • Ouabain
  • Strophanthidin
  • Oxidopamine
  • Dinoprost
  • Sodium-Potassium-Exchanging ATPase
  • acetylstrophanthidin
  • Norepinephrine