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Effects of the angiotensin II type 1 (AT1) receptor antagonist valsartan and the angiotensin-converting enzyme (ACE) inhibitor enalapril were studied in streptozotocine (STZ)-induced diabetes in rats on the basis of microalbuminuria (Ma) and renal morphology. Five groups of Wistar rats were used, one group was the non-diabetic control, one group consisted of untreated STZ-diabetics and 3 groups of STZ-diabetics were treated with either enalapril and/or valsartan for 30 days. Blood glucose (BG) and Ma levels, body and kidney weight and glomerular size were measured. Immunohistochemical staining with an anti-transforming growth factor-beta1 (TGF-beta1) antibody was performed as well. In STZ-diabetics, BG and Ma levels were significantly increased when compared with the non-diabetic group. Although Ma levels in the valsartan-treated group was found to be higher than those in the non-diabetics group after 15 days of treatment, in all treated diabetic groups Ma levels were significantly decreased as compared with STZ-diabetics at the end of the experiment. Thickening of the glomerular and tubular basement membranes, increased mesangial matrix and glomerular size were found in the untreated diabetic group. All these changes were less in the treated groups. A significant increase in TGF-beta1 immunoreactivity was found in glomeruli of untreated STZ-diabetics as compared with non-diabetics. Again, TGF-beta1 expression was decreased in the treated groups as compared with untreated STZ-diabetics. We conclude that valsartan and enalapril have renoprotective effects in diabetic nephropathy. A combined therapy has an advantage because lower dosages of these drugs can be used. Their beneficial effects are related to a blockade of the renin-angiotensin system (RAS) and a decrease in TGF-beta1 expression in glomeruli.

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austin.unimelb.edu.au

The role of the angiotensin type 2 (AT(2)) receptor in the pathogenesis of progressive renal injury has not been previously elucidated. The renal expression of the AT(1) and AT(2) receptors in subtotally nephrectomized rats (STNx) and the effects of AT(2) receptor blockade on renal injury were explored. Reduced renal expression of the AT(1) but not the AT(2) receptor was observed in STNx by reverse transcription-PCR, by in vitro autoradiography, and by immunohistochemical staining. The STNx rats were randomly assigned to AT(1) receptor antagonist valsartan, AT(2) receptor antagonist PD123319, or the combination of both for 4 wk. Increased proteinuria in STNx rats was reduced by PD123319 but to a lesser degree when compared with valsartan. Reduced gene and protein expression of the slit diaphragm protein nephrin was prevented by either valsartan or PD123319. Expression of osteopontin, proliferating cell nuclear antigen, and monocyte/macrophage infiltration was increased in STNx rats and was reduced by both AT(1) and AT(2) receptor antagonists. These effects of AT(2) receptor antagonism were observed in the presence of increased BP in STNx rats. These findings suggest that blockade of the AT(2) receptor alone confers a degree of renal protection; in particular, it seems that the combination of the AT(1) and AT(2) receptor antagonists may confer additive renal effects than either receptor antagonist as monotherapy.

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marionegri.it

BACKGROUND: Normalization of proteinuria and even regression of glomerulosclerosis seem to occur in progressive renal disease upon blockade of the renin-angiotensin system. Here we quantified the effect of a combination of an angiotensin converting enzyme (ACE) inhibitor and an angiotensin II (Ang II) receptor antagonist on renal function and structure in spontaneous overt nephropathy in male Munich Wistar Fromter (MWF) rats. METHODS: Three groups of MWF rats were used: group 1 was studied at 25 weeks to provide baseline renal function and structure; group 2 was followed until 40 weeks of age; group 3 was treated with lisinopril (40 mg/L) and valsartan (180 mg/L) in drinking water from 25 to 40 weeks. A group of untreated Wistar rats (group 4, 40 weeks) was used as the control. At the end of the study renal hemodynamics, kidney tissue morphology, accumulation of type III collagen and evaluation of interstitial inflammatory cells were performed. RESULTS: MWF rats spontaneously developed hypertension, proteinuria, glomerulosclerosis, interstitial volume expansion and protein cast accumulation. Combined treatment completely reversed protein excretion and ameliorated renal plasma flow and the glomerular ultrafiltration coefficient. The combined therapy was effective in halting progressive glomerulosclerosis, particularly in glomeruli with mild sclerotic lesions, and reduced interstitial volume expansion. Type III collagen accumulation and protein cast also were reversed. Infiltrating cells were massively present in the interstitium already at 25 weeks, and augmented at 40 weeks in untreated rats. Combined treatment reduced infiltrating cells to values comparable to normal controls. CONCLUSIONS: These data indicate that in animals with spontaneous overt nephropathy, Ang II antagonism normalized proteinuria, eliminated inflammatory cell infiltration, and ameliorated glomerular and tubular structural changes.

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