Regulation of Endothelin-Converting Enzyme 1 in Nephrotic Syndrome in Rats
| Autor: | Mika Ikebe, Yushi Nakayama, Kimio Tomita, Yuka Tashima, Hiroshi Nonoguchi, Kohei Shimada, Kazuhiko Tanzawa |
|---|---|
| Rok vydání: | 2004 |
| Předmět: |
Endothelin Receptor Antagonists
Male medicine.medical_specialty Nephrotic Syndrome Time Factors Physiology Endothelin converting enzyme 1 Kidney Glomerulus Endothelin-Converting Enzymes Puromycin Aminonucleoside Biology Peptide hormone Gene Expression Regulation Enzymologic Natriuresis Rats Sprague-Dawley Internal medicine Genetics medicine Animals Aspartic Acid Endopeptidases RNA Messenger education Cyclic GMP Endothelin-3 Sulfonamides education.field_of_study Proteinuria Endothelin-1 Metalloendopeptidases food and beverages Bosentan Glomerulonephritis Nephrons General Medicine medicine.disease Endothelin 1 Rats Endocrinology Nephrology Enzyme Induction medicine.symptom Endothelin receptor Nephrotic syndrome Atrial Natriuretic Factor |
| Zdroj: | Nephron Experimental Nephrology. 94:e137-e145 |
| ISSN: | 1660-2129 |
| DOI: | 10.1159/000072497 |
| Popis: | Background: Nephrotic syndrome is characterized by severe proteinuria and sodium and water retention. Although endothelin (ET) 1 can cause natriuresis or antinatriuresis, the role played by ET-1 in proteinuria and in sodium retention due to nephrotic syndrome remains unclear. Methods: We investigated the role played by the ET-1 system in sodium and water retention and in proteinuria in puromycin aminonucleoside induced nephrotic syndrome in rats using microdissected nephron segments, competitive polymerase chain reaction, and Western blot. Results: The expression of prepro ET-1, ET-converting enzyme 1 (ECE-1), and ET A receptor mRNAs, but not ET B receptor mRNA, in the glomeruli was increased in rats with nephrotic syndrome. The cGMP generation in the glomeruli induced by atrial natriuretic peptide and ET-1 was decreased, whereas the ET-3-induced cGMP generation was increased in rats with nephrotic syndrome. ECE-1 mRNA expression was increased not only in the glomeruli, but also in the thick ascending limbs and collecting ducts. The protein expression of ECE-1 was increased in the membrane fraction of the cortex and in the outer and the inner medulla of nephrotic rats. Blockade of ET A and B receptors by bosentan did not inhibit the occurrence of nephrotic syndrome. However, the administration of bosentan increased the urinary sodium excretion. Conclusion: These data suggest that an activated ET-1-ET A receptor pathway in glomeruli and/or an increased ECE-1 mRNA expression in distal segments may participate in sodium and water retention, but not in the occurrence of nephrotic syndrome. |
| Databáze: | OpenAIRE |
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