Anemia ameliorates progressive renal injury in experimental DOCA-salt hypertension
Autor: | Helen M. Lafferty, Julia L. Troy, Helmut G. Rennke, Diego L. Garcia, Sharon Anderson, Barry M. Brenner |
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Rok vydání: | 1991 |
Předmět: |
Male
medicine.medical_specialty Anemia Kidney Glomerulus Urology Hemodynamics Sodium Chloride Hematocrit urologic and male genital diseases hemic and lymphatic diseases medicine Animals Desoxycorticosterone Proteinuria medicine.diagnostic_test urogenital system business.industry Glomerulosclerosis Rats Inbred Strains General Medicine Phlebotomy medicine.disease female genital diseases and pregnancy complications Capillaries Rats Hypertension Renovascular Blood pressure Nephrology Erythropoietin medicine.symptom business medicine.drug |
Zdroj: | Journal of the American Society of Nephrology. 1:1180-1185 |
ISSN: | 1046-6673 |
DOI: | 10.1681/asn.v1101180 |
Popis: | To explore the role of systemic hematocrit in the vascular adaptations which characterize desoxycorticosterone-salt hypertension, studies were performed in three groups of rats with uninephrectomy, desoxycorticosterone administration, and 1% saline in the drinking water. One group received recombinant human erythropoietin to increase hematocrit, and another group was subjected to phlebotomy and fed a low-iron diet to induce anemia. Control rats exhibited systemic and glomerular capillary hypertension, proteinuria, and substantial glomerular sclerosis at 8 wk. Erythropoietin modestly increased hematocrit and blood pressure and substantially aggravated glomerular capillary pressure, proteinuria, and glomerular sclerosis. In contrast, reduction of hematocrit with a low-iron diet significantly attenuated systemic and glomerular hypertension, proteinuria, and sclerosis. It was concluded that the pace of progression of glomerular injury can be limited by chronic reduction in hematocrit, which effectively ameliorates both systemic and glomerular hypertension in this model of salt-sensitive hypertensive renal disease. |
Databáze: | OpenAIRE |
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