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