Inflammatory mediators and beta-adrenoceptor function.
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.
Raaijmakers
J A
JA
Department of Pulmonary Disease, State University Hospital, Utrecht, The Netherlands.
Beneker
C
C
van Geffen
E C
EC
Meisters
T M
TM
Pover
P
P
D001095:Arachidonic Acids / Q000378:metabolism / Q000502:physiology*; D000242:Cyclic AMP / Q000096:biosynthesis; D006801:Humans; D007249:Inflammation / Q000503:physiopathology*; D007975:Leukotriene B4 / Q000494:pharmacology; D008168:Lung / Q000187:drug effects / Q000378:metabolism; D008214:Lymphocytes / Q000378:metabolism; D010972:Platelet Activating Factor / Q000494:pharmacology; D011869:Radioligand Assay; D011943:Receptors, Adrenergic, beta / Q000187:drug effects / Q000378:metabolism*; D013189:SRS-A / Q000494:pharmacology
D001095:Arachidonic Acids; D010972:Platelet Activating Factor; D011943:Receptors, Adrenergic, beta; D013189:SRS-A; D007975:Leukotriene B4; D000242:Cyclic AMP