Abstract
Bordetella pertussis and in particular its cell wall constituent endotoxin induces a hyporesponsiveness of the coronary vascular beta2-adrenoceptor and a hyperreactivity of the alpha2-adrenoceptor in the guinea pig coronary vascular system [5]. In literature, much attention has been paid to betaadrenoceptor desensitization and several hypotheses have been proposed in order to explain the molecular mechanisms of this phenomenon [4]. The involvement of mediators other than catecholamines has been considered. Among these mediators, arachidonic acid and its metabolites have been suggested to play a role in desensitization of beta-adrenoceptors in various experimental designs [2, 3, 4]. Since endotoxin is a powerful stimulator of the immune system and thus initiates the biosynthesis of various inflammatory mediators among which are the arachidonic acid metabolites, it seems of particular interest to examine the hypothesis that arachidonic acid metabolites are involved in beta2-adrenoceptor impairment in the coronary vascular system of the guinea pig heart after endotoxin. Furthermore, these experiments might also elucidate the possible role of prostaglandin synthesis for alpha2-adrenoceptor hyperreactivity.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
