ACE-INHIBITION REDUCES PROTEINURIA, GLOMERULAR-LESIONS AND EXTRACELLULAR-MATRIX PRODUCTION IN A NORMOTENSIVE RAT MODEL OF IMMUNE-COMPLEX NEPHRITIS

被引：121
作者：
RUIZORTEGA, M
GONZALEZ, S
SERON, D
CONDOM, E
BUSTOS, C
LARGO, R
GONZALEZ, E
ORTIZ, A
EGIDO, J
机构：
[1] UNIV AUTONOMA MADRID, FDN JIMENEZ DIAZ, RENAL UNIT, MADRID, SPAIN
[2] BELLVITGE HOSP, DEPT PATHOL, RENAL UNIT, BARCELONA, SPAIN
来源：
KIDNEY INTERNATIONAL | 1995年 / 48卷 / 06期
关键词：
D O I：
10.1038/ki.1995.476
中图分类号：
R5 [内科学]; R69 [泌尿科学（泌尿生殖系疾病）];
学科分类号：
1002 ; 100201 ;
摘要：
We studied the effect of the angiotensin converting enzyme (ACE) inhibitor, quinapril, on the clinical and morphological lesions of a normotensive model of immune complex nephritis. Untreated rats developed massive nephrotic syndrome, intense cell proliferation and glomerular and tubulointerstitial lesions. In the renal cortex of nephritic rats there was a significant increase in gene expression of TGF-beta 1, fibronectin and collagens, and ACE activity. Systolic blood pressure remained normal with progression of the disease. Administration of quinapril for three weeks to animals with glomerular lesions (proteinuria 20 to 50 mg/day) avoided the development of intense proteinuria (79 +/- 28 vs. 589 +/- 73 mg/day, P < 0.001) and decreased cell proliferation, glomerulosclerosis, tubulointerstitial lesions, and inflammatory infiltrates. Cortical gene expression of TGF-beta 1 and matrix proteins was also diminished. ACE activity was inhibited by 68% in renal cortex. These results show that quinapril administration to normotensive rats with immune complex nephritis decreases proteinuria and glomerular and tubulointerstitial lesions, probably modulating the local angiotensin II generation and its effects on cell growth, TGF beta and matrix protein synthesis.
引用
收藏
页码：1778 / 1791
页数：14
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