Inflammatory mediators and beta-adrenoceptor function

Agents Actions. 1989 Jan;26(1-2):45-7. doi: 10.1007/BF02126558.

Abstract

In this study the, in vitro, influence of arachidonic acid metabolites on human beta-adrenoceptors was investigated. Incubation of normal human pulmonary membranes with PAF, LTB4 and LTC4 affected pulmonary beta-adrenoceptor properties, as was shown in radioligand binding studies. The same mediators were able to induce a decreased lymphocyte cAMP synthesis. It is concluded that beta-adrenoceptor deficiencies, that can be demonstrated in peripheral lung tissue of COLD patients, may result from pathological processes such as inflammation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Arachidonic Acids / metabolism
  • Arachidonic Acids / physiology*
  • Cyclic AMP / biosynthesis
  • Humans
  • Inflammation / physiopathology*
  • Leukotriene B4 / pharmacology
  • Lung / drug effects
  • Lung / metabolism
  • Lymphocytes / metabolism
  • Platelet Activating Factor / pharmacology
  • Radioligand Assay
  • Receptors, Adrenergic, beta / drug effects
  • Receptors, Adrenergic, beta / metabolism*
  • SRS-A / pharmacology

Substances

  • Arachidonic Acids
  • Platelet Activating Factor
  • Receptors, Adrenergic, beta
  • SRS-A
  • Leukotriene B4
  • Cyclic AMP