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Am J Physiol Regul Integr Comp Physiol 274: R1797-R1806, 1998;
0363-6119/98 $5.00
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Vol. 274, Issue 6, R1797-R1806, June 1998

Effects of chronic inhibition of ACE and AT1 receptors on glomerular injury in Dahl salt-sensitive rats

Fumio Otsuka1, Takayoshi Yamauchi2, Hideo Kataoka1, Yukari Mimura1, Toshio Ogura2, and Hirofumi Makino1

1 Department of Medicine III, Okayama University Medical School, and 2 Health and Medical Center, Okayama University, Okayama 700-8558 Japan

To elucidate the contribution of the renin-angiontensin system (RAS) to glomerular injury in salt-sensitive hypertension, we investigated the chronic effects of the angiotensin I-converting enzyme inhibitor cilazapril and the angiotensin II type 1-receptor antagonist (AT1a) TCV-116 in Dahl-Iwai rats. Dahl salt-sensitive (S) rats receiving 8% salt diet for 6 wk were simultaneously treated with cilazapril (n = 6), TCV-116 (n = 6), or saline (n = 14). The 8% salt diet markedly increased systolic blood pressure (SBP), urinary protein, and N-acetyl-beta -glucosaminidase (NAG) excretion compared with 0.3% salt-treated S (n = 6) or salt-resistant (n = 6) rats. Although neither cilazapril nor TCV-116 reduced the elevated SBP, TCV-116 significantly lowered urinary protein and NAG excretion. Histologically, 8% salt treatment in S rats induced progressive sclerotic and proliferative glomerular changes, which were ameliorated by both drugs. TCV-116 increased the glomerular diameter. Immunofluorescence demonstrated the increased level of type III collagen in the mesangium of 8% salt-treated S rats, which was completely reversed by TCV-116. Competitive RT-PCR of mRNA extracted from the glomeruli revealed that 8% salt treatment significantly increased the levels of proliferating cell nuclear antigen (PCNA) and platelet-derived growth factor B-chain and that TCV-116 significantly reduced the levels of PCNA and transforming growth factor-beta 1 (TGF-beta 1). Thus, although the chronic RAS-inhibition in salt-sensitive hypertension exerted a histologically renoprotective effect by both ways without lowering blood pressure, the RAS inhibition due to AT1a had more beneficial advantages of reducing proteinuria and attenuating the levels of glomerular TGF-beta 1 and extracellular matrix.

glomerulosclerosis; type III collagen; transforming growth factor-beta 1; proliferating cell nuclear antigen; platelet-derived growth factor B-chain


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