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Effects of dexamethasone and indomethacin on the vascularβ2-adrenolytic action of pertussis toxin in rats; A prostaglandin-mediated phenomenon

Authors
Journal
European Journal of Pharmacology
0014-2999
Publisher
Elsevier
Publication Date
Volume
108
Issue
2
Identifiers
DOI: 10.1016/0014-2999(85)90715-0
Keywords
  • Pertussis Toxin
  • β2-Adrenoceptor
  • Indomethacin
  • Dexamethasone
  • Cardiovascular System
  • Rat

Abstract

Abstract Lymphocytosis promoting factor (LPF), alternatively described as pertussis toxin, inhibits the vasodilation after β 2-adrenoceptor stimulation with salbutamol as well as the negative chronotropic activity induced by the muscarinic receptor stimulant arecoline 4 days after vaccination of rats. To analyse whether arachidonic acid metabolites contributed to these phenomena the cyclo-oxygenase inhibitor indomethacin and the phospholipase A 2 inhibitor dexamethasone were administered over a period of 4 days. Pretreatment with either drug restored β 2-adrenoceptor responsiveness. The cardiac anticholinergic effect, however, was not changed. Interestingly, neither of the inhibitors prevented the blood pressure lowering effect of LPF. The reversing effect on vascular β 2-hyporesponsiveness of indomethacin and dexamethasone therefore appears to be rather specific. It is concluded that endogenous prostaglandins may participate in the vascular β 2-adrenergic impairment caused by LPF. Furthermore, the results are considered in view of desensitization theories and underlying mechanisms of LPF-induced autonomic impairment.

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