Effects of dexamethasone and indomethacin on the vascular β2-adrenolytic action of pertussis toxin in rats; A prostaglandin-mediated phenomenon
Autor: | Dick J. De Wildt, Yeb De Jong, Johan G. Kreeftenberg, Frans P. Nijkamp, Eline Marleen Van Der Beek |
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Rok vydání: | 1985 |
Předmět: |
Male
medicine.medical_specialty Bordetella pertussis Adrenergic beta-Antagonists Bacterial Toxins Indomethacin Prostaglandin Blood Pressure Vasodilation Pertussis toxin Dexamethasone chemistry.chemical_compound Heart Rate Internal medicine Muscarinic acetylcholine receptor Animals Medicine Drug Interactions Arecoline Virulence Factors Bordetella Pharmacology Dose-Response Relationship Drug biology business.industry Parasympatholytics Rats Inbred Strains Prostaglandin antagonist biology.organism_classification Rats Endocrinology Pertussis Toxin chemistry Prostaglandins Blood Vessels business medicine.drug |
Zdroj: | European Journal of Pharmacology. 108:113-119 |
ISSN: | 0014-2999 |
DOI: | 10.1016/0014-2999(85)90715-0 |
Popis: | Lymphocytosis promoting factor (LPF), alternatively described as pertussis toxin, inhibits the vasodilation after beta 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 A2 inhibitor dexamethasone were administered over a period of 4 days. Pretreatment with either drug restored beta 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 beta 2-hyporesponsiveness of indomethacin and dexamethasone therefore appears to be rather specific. It is concluded that endogenous prostaglandins may participate in the vascular beta 2-adrenergic impairment caused by LPF. Furthermore, the results are considered in view of desensitization theories and underlying mechanisms of LPF-induced autonomic impairment. |
Databáze: | OpenAIRE |
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