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Graier, WF; Schmidt, K; Kukovetz, WR.
Is the bradykinin-induced Ca2+ influx and the formation of endothelium-derived relaxing factor mediated by a G protein?
Eur J Pharmacol. 1992; 225(1):43-49
Doi: 10.1016/0922-4106(92)90037-V
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- Leading authors Med Uni Graz
- Graier Wolfgang
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- Abstract:
- In cultured porcine aortic endothelial cells bradykinin produced a long-lasting Ca2+ influx. In contrast to the G protein-independent Ca2+ entry evoked by ionomycin or digitonin, bradykinin-induced Ca2+ influx was antagonized by Ni2+ with an IC50 value of about 50 microM. Since identical IC50 values for Ni2+ were found when Ca2+ entry was induced by sodium fluoride or GTP gamma S, we suggest that stimulation of G protein(s) results in the activation of the same Ca2+ channels as stimulation by bradykinin. This conclusion is supported by our findings that inhibition of GTPase by mepacrine amplified bradykinin-stimulated Ca2+ influx, but did not interfere with the effect of the Ca2+ ionophore A23187. Similar to its effect on Ca2+ influx, mepacrine also potentiated endothelium-derived relaxing factor (EDRF) formation by bradykinin and sodium fluoride, but did not affect A23187-induced EDRF biosynthesis. We therefore suggest that in endothelial cells the bradykinin-induced Ca2+ influx and the resulting formation of EDRF are regulated by a G protein.
- Find related publications in this database (using NLM MeSH Indexing)
- Animals -
- Bradykinin - pharmacology
- Calcimycin - pharmacology
- Calcium - metabolism
- Cells, Cultured - metabolism
- Cyclic GMP - analysis
- Endothelium, Vascular - drug effects
- GTP-Binding Proteins - physiology
- Guanosine 5'-O-(3-Thiotriphosphate) - pharmacology
- Nickel - pharmacology
- Nitric Oxide - biosynthesis
- Sodium Fluoride - pharmacology
- Swine - pharmacology
- Find related publications in this database (Keywords)
- BRADYKININ
- ENDOTHELIAL CELLS
- CA2+ CHANNELS
- G-PROTEIN
- ENDOTHELIUM-DERIVED RELAXING FACTOR (EDRF)
- CGMP