Modulation of prostacyclin biosynthesis by calcium entry blockers and extracellular calcium
| Autor: | Hidde Bult, Arnold G. Herman, V. Van de Velde, Rita M. Van den Bossche |
|---|---|
| Rok vydání: | 1986 |
| Předmět: |
medicine.medical_specialty
chemistry.chemical_element Bradykinin Prostacyclin 6-Ketoprostaglandin F1 alpha Calcium Phospholipase Biochemistry Membrane Potentials chemistry.chemical_compound Nifedipine Internal medicine medicine Extracellular Animals Calcimycin Cells Cultured Pharmacology Chemistry Thrombin Calcium Channel Blockers Epoprostenol Endocrinology Verapamil Rabbits Peritoneum Intracellular medicine.drug |
| Zdroj: | Biochemical pharmacology. 35(2) |
| ISSN: | 0006-2952 |
| Popis: | The influence of variations in the availability of extracellular Ca 2+ and of Ca 2+ -entry blockers on prostacyclin production by mesothelial cells in culture was studied. The Ca 2+ -entry blockers nifedipine and verapamil suppressed the basal, as well as the thrombin-, bradykinin-, and ionophore A23187-stimulated biosynthesis by about 50–60%, but high concentrations were required and the inhibition was never complete. Basal prostacyclin formation was unaffected by a Ca 2+ -poor buffer, but showed 50% reduction in the Ca 2+ -free buffer. Although the thrombin-stimulated prostacyclin formation was not significantly influenced by a Ca 2+ -poor or a Ca 2+ -free buffer, prostacyclin release stimulated by A23187 and bradykinin was diminished in the presence of these modified incubation media; the reduction of bradykinin stimulated biosynthesis was rather small (30%). These results suggest that the Ca 2+ from intracellular stores is sufficient for half maximal stimulation of the phospholipases involved in the biosynthetic pathway of prostacyclin and that—depending on the nature of the stimulus—different phospholipases are activated with varying requirements for free Ca 2+ . |
| Databáze: | OpenAIRE |
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