Bradykinin synergistically potentiates interleukin-1 induced bone resorption and prostanoid biosynthesis in neonatal mouse calvarial bones |
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| Authors: | U H Lerner |
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| Institution: | 1. Institute of Pharmacology and Clinical Pharmacology, Heinrich Heine University, Düsseldorf, Germany;2. Institute of Clinical Pharmacology, Goethe University, Frankfurt/Main, Germany;3. Institute of Forensic Medicine, Heinrich Heine University, Düsseldorf, Germany;4. Institute of Pharmaceutical and Medicinal Chemistry, University of Münster, Münster, Germany;1. Institute of Pharmacology andClinical Pharmacology, University Hospital, Heinrich Heine University, Düsseldorf, Germany;2. Department of Oto-Rhino-Laryngology, Head and Neck Surgery, Ulm University Medical Center, Germany;3. Otorhinolaryngology Department, University Hospital Rechts der Isar, Munich Technical University, Munich, Germany |
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| Abstract: | Interleukin-1 (IL-1) alpha and beta dose-dependently stimulated the release of 45Ca and the formation of prostaglandin E2 (PGE2) and PGI2 in cultured mouse calvarial bones, with IL-1 beta being the most potent agonist. Bradykinin (BK; 10 nmol/l) synergistically potentiated the effect of IL-1 alpha (10 pg/ml) and IL-1 beta (5 pg/ml) both on 45Ca release and on biosynthesis of PGE2 and PGI2. The capacity of BK to potentiate IL-1 beta induced 45Ca release and PGE2 formation was seen at concentrations of BK from 1-1000 nmol/l. These data indicate that BK and IL-1, which are formed in inflammatory processes, may act in concert to stimulate bone resorption in the vicinity of inflammatory lesions. |
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