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Graier, WF; Schmidt, K; Kukovetz, WR.
Bradykinin-induced Ca(2+)-influx into cultured aortic endothelial cells is not regulated by inositol 1,4,5-trisphosphate or inositol 1,3,4,5-tetrakisphosphate.
Second Messengers Phosphoproteins. 1991; 13(4):187-197
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- Leading authors Med Uni Graz
- Graier Wolfgang
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- Abstract:
- Since inositol 1,4,5-trisphosphate (1,4,5-IP3) and inositol 1,3,4,5-tetrakisphosphate (1,3,4,5-IP4) have been described to modulate Ca(2+)-channels, we investigated the possible participation of 1,4,5-IP3 and/or 1,3,4,5-IP4 in the bradykinin-induced Ca(2+)-influx into cultured porcine aortic endothelial cells. In our experiments bradykinin induced a quick release of Ca2+ from intracellular stores and a longlasting Ca(2+)-influx, which remained constant for at least 15 minutes. In contrast to its effect on [Ca2+]i, bradykinin only transiently elevated 1,4,5-IP3 and 1,3,4,5-IP4 levels. Ten minutes after addition of bradykinin, both 1,4,5-IP3 and 1,3,4,5-IP4 levels returned to basal values, whereas Ca(2+)-influx was still unaltered. Furthermore, preincubation of endothelial cell with phorbol-12-myristate-13-acetate (PMA) abolished the stimulatory effect of bradykinin on the formation of 1,4,5-IP3 and 1,3,4,5-IP4, but did not affect the longlasting Ca(2+)-influx. These data provide evidence that in endothelial cells inositolphosphates are not involved in the regulation of bradykinin-induced longlasting Ca(2+)-influx.
- Find related publications in this database (using NLM MeSH Indexing)
- Animals -
- Aorta - drug effects
- Bradykinin - pharmacology
- Calcium - metabolism
- Cells, Cultured - metabolism
- Endothelium, Vascular - drug effects
- Inositol 1,4,5-Trisphosphate - physiology
- Inositol Phosphates - physiology
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