Mechanisms involved in the progression to glomerular sclerosis induced by systemic hypertension during mild puromycin aminonucleoside nephrosis
Autor: | Martha Franco, Romeo García-Tones, Edilia Tapia, Dante Amato, Jaime Herrera-Acost, Consuelo Calleja, Pedro Lόpez, J. Alfredo Alvarado, Norma A. Bobadilla |
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Rok vydání: | 1992 |
Předmět: |
Male
medicine.medical_specialty Nephrosis Kidney Glomerulus Hemodynamics Blood Pressure Puromycin Aminonucleoside urologic and male genital diseases Nephropathy Internal medicine Internal Medicine medicine Animals Rats Wistar Triglycerides Proteinuria Sclerosis urogenital system business.industry Glomerulosclerosis Lipid metabolism medicine.disease Rats Disease Models Animal Endocrinology Blood pressure Cholesterol Hypertension Renovascular medicine.symptom Complication business |
Zdroj: | American journal of hypertension. 5(9) |
ISSN: | 0895-7061 |
Popis: | To evaluate the contribution of systemic hypertension in the progression of nephropathies to glomerular sclerosis, a mild form of puromycin aminonucleoside (PAN) nephrosis was associated with Goldblatt hypertension and studied after 18 weeks. We studied four groups: Group I, controls; Group II, Goldblatt hypertension; Group III, PAN nephrosis; and Group IV, both conditions. Systolic blood pressure, 24-h proteinuria, serum cholesterol, triglycerides, glomerular hemodynamics, and histological studies were compared among the groups. Rats in groups II and IV developed systemic hypertension, but only group IV rats showed persistent proteinuria. No alterations in lipid metabolism were present in any of the groups. The most striking findings in the micropuncture studies were a significant increase of glomerular capillary pressure in group IV rats (63.15 +/- 1.34 mm Hg) as compared to controls (48.74 +/- 0.97 mm Hg) and to groups II and III (55.31 +/- 2.11 and 48.17 +/- 1.23 mm Hg, respectively), and a marked fall in Kf in groups III and IV. Only group IV showed significant histological alterations such as glomerular sclerosis, interstitial damage, and increased glomerular area. These results suggest that, in the presence of an underlying nephropathy, a greater fraction of systemic pressure is transmitted to the glomerular capillaries when systemic hypertension is present; the resulting elevation in glomerular pressure and proteinuria seems to be responsible for the progression to glomerular sclerosis. |
Databáze: | OpenAIRE |
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