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      Role of Kinins in the Renoprotective Effect of Angiotensin–Converting Enzyme Inhibitors in Experimental Chronic Renal Failure

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          The aim of this study was to investigate whether the renoprotective effect of angiotensin–converting enzyme inhibitors (ACEIs) following 5/6 renal mass reduction is due in part to the potentiation of kinins. Three groups of rats with 5/6 renal mass reduction were studied during the 14 weeks following surgery. One group received no therapy (control); the second group was treated from the beginning with the ACEI ramipril (1 mg/kg/day) added to the drinking water, and the last group received ramipril plus a β<sub>2</sub>–bradykinin antagonist, HOE 140 (500 μg/kg/day) via osmotic minipumps. Plasma creatinine did not change in any group during the study. Urinary protein excretion rose in the controls from 9.18±1.6 to 45.0±5.6 mg/24 h at the end of the study. In ramipril group proteinuria was prevented (initial 7.5±1.0 and final 8.6±0.8 mg/24h). The effect of ramipril was abolished by HOE 140 (initial 11.6±2.0 and final 38.9±11 mg/ 24h). The systolic blood pressure of the controls increased from 106±2 to 144±5mmHg at the 14th week. Ramipril abolished the increase in systolic blood pressure. The effect of ramipril was reverted by HOE 140 (initial 108±2 and final 140±9 mmHg). Control rats had more severe histopathologic changes. Those animals receiving ramipril + HOE 140 displayed less severe glomerular changes, while rats treated only with ramipril had mild alterations. Thus the glomerular injury score was 2.11±0.32 for controls, 1.53±0.52 for rats treated with ramipril + HOE 140, and 0.06±0.04 for rats treated only with ramipril. The glomerular area was 20,886±1,410, 19,693±2,200 and 14,352±3,200 μm<sup>2</sup>, respectively, for the 3 groups. These results suggest that the protective effect of ACEIs in the development of chronic renal failure is partially mediated by kinins.

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          Reduction of infarct size by local angiotensin-converting enzyme inhibition is abolished by a bradykinin antagonist.

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            Reduction of myocardial infarct size by ramiprilat is independent of angiotensin II synthesis inhibition


              Author and article information

              Kidney Blood Press Res
              Kidney and Blood Pressure Research
              S. Karger AG
              12 November 1998
              : 21
              : 5
              : 329-334
              aInstituto de Investigaciones Cardiológicas y bDepartamento de Patologia Facultad de Medicina, Universidad de Buenos Aires, Argentina
              25890 Kidney Blood Press Res 1998;21:329–334
              © 1998 S. Karger AG, Basel

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              Figures: 3, Tables: 1, References: 32, Pages: 6
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