Thapsigargin increases cellular free calcium and intracellular sodium concentrations in cultured rat glomerular mesangial cells
Autor: | T. Saito, K. Okada, G. Fujisawa, S.-E. Ishikawa |
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Rok vydání: | 1993 |
Předmět: |
Male
medicine.medical_specialty Thapsigargin Time Factors Renal glomerulus Biophysics chemistry.chemical_element Calcium-Transporting ATPases Calcium Biochemistry Rats Sprague-Dawley chemistry.chemical_compound Internal medicine medicine Animals Channel blocker Molecular Biology Ion transporter Cells Cultured Mesangial cell Chemistry Terpenes Endothelins Sodium Cell Biology Hydrogen-Ion Concentration Glomerular Mesangium Rats Calcium ATPase Arginine Vasopressin EGTA Kinetics Endocrinology cardiovascular system |
Zdroj: | Biochemical and biophysical research communications. 194(1) |
ISSN: | 0006-291X |
Popis: | We examined whether thapsigargin increases cellular free calcium ([Ca 2+ ]i) and intracellular sodium concentration ([Na + ]i) in cultured rat glomerular mesangial cells. 1 × 10 −6 M Thapsigargin increased [Ca 2+ ]i to 244.4 from 86.6 nM, an increase sustained at least during the 15 min observation period. Such an increase in [Ca 2+ ]i was transient in Ca 2+ -free medium containing 1 x 10 −4 M EGTA. An increase in [Ca 2+ ]i by thapsigargin was not altered by 1 x 10 −6 M nicardipine, a L-type Ca 2+ channel blocker. Thapsigargin also produced a sustained rise in [Na + ]i in a dose-dependent manner. However, preincubation of cells with Ca 2+ -free medium completely blocked the increase in [Na + ]i by thapsigargin. These results indicate that thapsigargin increases [Ca 2+ ]i by blocking endoplasmic Ca 2+ -ATPase and enhancing Ca 2+ entry, and that the increased Ca 2+ influx is triggering an increase in [Na + ]i stimulated by thapsigargin per se in glomerular mesangial cells. |
Databáze: | OpenAIRE |
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