Urinary calcium excretion and renal calbindin-D28k
| Autor: | Michael Staun, Klaus Olgaard, Kirsten Bang, Claus Hemmingsen, Karen Meibom |
|---|---|
| Rok vydání: | 1997 |
| Předmět: |
Male
medicine.medical_specialty Calbindins Sodium Chloride Symporter Inhibitors chemistry.chemical_element Calcium Benzothiadiazines Kidney Excretion Cytosol S100 Calcium Binding Protein G Internal medicine medicine Animals Rats Wistar Diuretics Thiazide Chemistry General Medicine Urinary calcium Rats Endocrinology Nephrology Calbindin 1 Calbindin d28k Cardiology and Cardiovascular Medicine medicine.drug |
| Zdroj: | Europe PubMed Central |
| ISSN: | 1420-4096 |
| Popis: | The present investigation examined the possible influence of urinary calcium excretion on the concentration of renal calbindin-D28k. Thiazide diuretics stimulate calcium transport across the epithelial cells of the distal tubule, which express calbindin-D28k in high concentrations. Calbindin-D28k is assumed to facilitate transcellular Ca diffusion. Reduced urine calcium excretion and increased urine output were induced in Wistar rats by infusion of bendroflume-thiazide 1 mg/kg/day. The two control groups had infusions of either furosemide 20 mg/kg/day or vehicle, n = 8 in each group. Urinary Ca excretion was reduced to 10% in the thiazide group and increased by 50% in the furosemide group. Renal concentrations of calbindin-D28 showed no difference between vehicle, thiazide- and furosemide-treated rats. No differences in plasma concentrations of calcium, magnesium, phosphorus, urea, PTH, calcitonin and 1,25-(OH)2D were found between the groups. The present study describes that urine calcium excretion selectively can be manipulated without accompanying changes in renal calbindin-D28k concentrations. The data, therefore, suggest that urinary calcium excretion is not a significant determinator of cytosolic concentrations of renal calbindin-D28k. |
| Databáze: | OpenAIRE |
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