Autocrine Production of Endothelin-1 Participates in the Glucocorticoid-Induced Ca2+ Influx into Vascular Smooth Muscle Cells
| Autor: | Takio Hayashi, Koji Oida, Tsuguhiko Nakai, Yusuke Koshino, Yasunori Kutsumi, H. Kato, Susumu Miyabo |
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| Rok vydání: | 1995 |
| Předmět: |
Endothelin Receptor Antagonists
Dihydropyridines medicine.medical_specialty Indoles Vascular smooth muscle Biophysics Biology Biochemistry Dexamethasone Muscle Smooth Vascular Cell Line Internal medicine medicine Animals Carbon Radioisotopes Autocrine signalling Protein kinase A Receptor Molecular Biology Aorta Receptors Endothelin Endothelins Dihydropyridine Biological Transport Azepines Cell Biology Endothelin 1 Rats Kinetics Endocrinology Cell culture cardiovascular system Calcium Isradipine Endothelin receptor medicine.drug |
| Zdroj: | Biochemical and Biophysical Research Communications. 208:82-88 |
| ISSN: | 0006-291X |
| DOI: | 10.1006/bbrc.1995.1308 |
| Popis: | We determined whether endothelin-1 (ET-1) is associated with glucocorticoid-induced Ca2+ influx into vascular smooth muscle cells by examining the effects of the ETA receptor antagonist FR139317 on dexamethasone-induced 45Ca2+ uptake and dihydropyridine binding by rat A7r5 cells. FR139317 inhibited the dexamethasone-induced 45Ca2+ uptake and [methyl-3H]PN 200-110 binding in a dose-dependent manner. Slot blot analysis revealed that dexamethasone increased protein kinase C-alpha in A7r5 cells and that this effect was also abolished by FR139317. Dexamethasone stimulated the release of immunoreactive endothelin-1 from A7r5 cells into the culture medium. These results suggest that endothelin participates in the glucocorticoid-induced Ca2+ influx through dihydropyridine-sensitive channels in an autocrine manner, possibly linked to the activation of protein kinase C-alpha. |
| Databáze: | OpenAIRE |
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