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• W2014906900 abstract "Aldosterone at physiological levels induces rapid (<5 min) increases in intracellular protein kinase C (PKC) activity and a rise in calcium and pH in mineralocorticoid hormone target epithelia, such as distal colon and sweat gland. The end targets of these rapid responses in epithelia are Na+/H+ exchange and K+ channels.The mouse cortical collecting duct (CCD) M-1 cell line was grown to confluency and loaded with Fura-2 for spectrofluorescence measurements of intracellular free calcium at 37 degrees C bathed in Krebs solution.Aldosterone (1 nmol/L) produced a rapid, transient peak increase in [Ca2+]i in M-1 cells. This effect was abolished upon removal of extracellular Ca2+, but was unaffected by pretreatment with spironolactone (10 micromol/L) or actinomycin D (10 micromol/L). However, pretreatment with the specific PKC inhibitor chelerythrine chloride (1 micromol/L) prevented the aldosterone-induced rise in [Ca2+]i. Dexamethasone, at a concentration 10,000-fold higher than aldosterone (10 micromol/L), also produced a transient increase in [Ca2+]i, but this response was significantly smaller than that of aldosterone. In contrast, hydrocortisone had no effect on [Ca2+]i at either nmol/L or micromol/L concentrations. Both of the sex steroids, 17beta-estradiol (10 nmol/L) and progesterone (10 nmol/L), induced protein kinase C-dependent increases in [Ca2+]i.Aldosterone and sex steroid hormones activate intracellular calcium signaling in CCD cells via a nongenomic PKC-dependent pathway, which may have important implications for renal transport." @default.
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• W2014906900 date "2000-04-01" @default.
• W2014906900 modified "2023-09-25" @default.
• W2014906900 title "Nongenomic effects of aldosterone on Ca2+ in M-1 cortical collecting duct cells" @default.
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• W2014906900 doi "https://doi.org/10.1046/j.1523-1755.2000.00981.x" @default.
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