Stimulation of bone resorption in cultured mouse calvaria by Lys-bradykinin (kallidin), a potential mediator of bone resorption linking anaphylaxis processes to rarefying osteitis.
Lys-Bradykinin (kallidin) stimulated bone resorption in vitro as assessed by the release of 45Ca and 3H from mouse calvaria radiolabelled in vivo with [45Ca]CaCl2 and [3H]proline, respectively. The stimulatory effect of Lys-bradykinin was reduced by calcitonin, indicating that the bone resorptive effect of Lys-bradykinin was dependent on osteoclastic activity. Different inhibitors of arachidonic acid metabolism, including glucocorticoids, inhibited Lys-bradykinin stimulated mobilization of mineral, implicating the synthesis of prostaglandins as an intermediary step. Lys-Bradykinin enhanced the biosynthesis of PGE2 in osteoblast-like cells isolated from mouse calvaria. In view of these findings and the capacity of mast cells to generate kininogenase activity, resulting in formation of Lys-bradykinin and bradykinin, the role of these cells in the pathogenesis of bone loss in rheumatoid arthritis, mastocytosis and osteoporosis is discussed.
D000707:Anaphylaxis / Q000209:etiology; D000818:Animals; D001862:Bone Resorption / Q000187:drug effects*; D001842:Bone and Bones / Q000187:drug effects / Q000378:metabolism; D002118:Calcium / Q000378:metabolism; D015232:Dinoprostone / Q000494:pharmacology; D066298:In Vitro Techniques; D007609:Kallidin / Q000494:pharmacology*; D008407:Mast Cells / Q000187:drug effects / Q000378:metabolism; D051379:Mice; D010000:Osteitis / Q000209:etiology; D010281:Parathyroid Hormone / Q000494:pharmacology
D010281:Parathyroid Hormone; D007609:Kallidin; D015232:Dinoprostone; D002118:Calcium