The presence of genetic hypertension stimulates early renal accumulation of fibronectin in experimental diabetes mellitus

• Published in: Diabetologia 2001-11, Vol.44 (11), p.2088-2091
• Main Authors: RIGHETTI, A. E, BOER-LIMA, P. A, LOPES DE FARIA, J. B
• Format: Article
• Language: English
• Subjects: Animals; Antibodies; Associated diseases and complications; Biological and medical sciences; Blood Glucose - metabolism; Blood Pressure; Diabetes; Diabetes Mellitus, Experimental - blood; Diabetes Mellitus, Experimental - physiopathology; Diabetes. Impaired glucose tolerance; Diabetic nephropathy; Endocrine pancreas. Apud cells (diseases); Endocrinopathies; Fibronectins - metabolism; Hyperglycemia; Hypertension; Hypertension - genetics; Kidney - pathology; Kidney - physiopathology; Kidney diseases; Laboratory animals; Lasers; Medical research; Medical sciences; Microscopy; Microscopy, Confocal; Morphology; Nephrology; Proteins; Rats; Rats, Inbred SHR; Rats, Inbred WKY
• ISSN: 0012-186X; 1432-0428
• DOI: 10.1007/s001250100014

To investigate the interaction between hypertension and diabetic nephropathy, we studied the renal accumulation of fibronectin in a genetic model of hypertension with streptozotocin-induced diabetes mellitus. Spontaneously hypertensive rats (SHR) and their genetically normotensive control Wistar Kyoto rats (WKY) were studied at 4 weeks of age. The rats were killed 20 days after the induction of diabetes mellitus. The renal accumulation of fibronectin was estimated using Western blot analysis as well as immunofluorescence technique and confocal microscopy. Blood glucose concentrations were similar in diabetic SHR rats (27 +/- 3.3 mmol/l) and WKY rats (25.5 +/- 2.7 mmol/l). The systolic blood pressure was higher in both groups of SHR rats than in the control rats. The abundance of renal fibronectin as detected by Western blot analysis was (p < 0.05) higher in the diabetic SHR rats (41.4 +/- 15.0 densitometric U, n = 8) than in the control rats, and no difference was observed between diabetic and control WKY rats (20.8 +/- 6.2, n = 8) and (27.8 +/- 17.2, n = 8). The mean peak intensity of fibronectin signal within the glomerulus as estimated by confocal microscopy was higher (p < 0.05) in the diabetic SHR rats (32.9 +/- 3.5) than in control SHR rats (11.9 +/- 5.7) or diabetic (7.4 +/- 2.2) and control (15.2 +/- 7.9) WKY rats. In experimental diabetes the presence of genetic hypertension promotes earlier accumulation of renal fibronectin, a matrix protein implicated in renal glomerulosclerosis.