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      Angiotensin-Converting Enzyme Inhibition Attenuates Hypercholesterolemia and Glomerular Injury in Hyperlipidemic Imai Rats

      a , b , b


      S. Karger AG

      Enalapril, Glomerulosclerosis, Spontaneous hypercholesterolemia

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          Hyperlipidemic Imai rats spontaneously develop hypercholesterolemia, proteinuria and glomerulosclerosis. We investigated the effect of enalapril, an angiotensin-converting enzyme (ACE) inhibitor, on spontaneous hypercholesterolemia and the progressive renal injury in this rat strain. Male Imai rats (n = 7) were treated with enalapril at a dose of 50 mg/l in drinking water starting at 6 weeks of age. Body weight, blood pressure, urinary protein excretion and serum constituents were checked and compared with untreated controls (n = 5) up to 38 weeks of age. Enalapril treatment significantly reduced hypercholesterolemia (247 ± 41 vs. 102 ± 13 mg/d1, p < 0.01, at 38 weeks) and proteinuria (766 ± 290 vs. 206 ± 119 mg/kg/day, p < 0.01, at 38 weeks). The glomerulosclerosis index (SI) was significantly higher in untreated control rats than in the enalapril-treated group (227 ± 57 vs. 27 ± 9, p < 0.01). Although we could not clarify whether hypercholesterolemia is a primary event or secondary to the nephrotic syndrome, these results indicate that the ACE inhibitor has the property to protect remnant glomeruli from glomerulosclerosis in male Imai rats as well as in other animal models in which focal and segmental glomerulosclerosis is believed to represent a common pathologic pattern. This rat strain represents a unique model of a spontaneous proteinuria which can provide an important information on the pathogenesis of human focal and segmental glomerulosclerosis.

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          Author and article information

          S. Karger AG
          12 December 2008
          : 62
          : 3
          : 315-321
          Departments of aInternal Medicine and bPathology, Saga Medical School, Saga, Japan
          187066 Nephron 1992;62:315–321
          © 1992 S. Karger AG, Basel

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          Pages: 7
          Original Paper


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