Effects of modulation of renal kallikrein-kinin system in the nephrotic syndrome
| Autor: | Victor I. Martin, Florence N. Hutchison |
|---|---|
| Rok vydání: | 1990 |
| Předmět: |
Male
medicine.medical_specialty Nephrotic Syndrome Physiology Blood Pressure Kinins Kidney urologic and male genital diseases Plasma renin activity chemistry.chemical_compound Aprotinin Enalapril Internal medicine Renin Renin–angiotensin system medicine Albuminuria Animals Serum Albumin biology urogenital system Phosphoramidon Glycopeptides Rats Inbred Strains Angiotensin-converting enzyme Kinin Angiotensin II female genital diseases and pregnancy complications Rats Endocrinology chemistry biology.protein Kallikreins Neprilysin hormones hormone substitutes and hormone antagonists circulatory and respiratory physiology medicine.drug |
| Zdroj: | American Journal of Physiology-Renal Physiology. 258:F1237-F1244 |
| ISSN: | 1522-1466 1931-857X |
| DOI: | 10.1152/ajprenal.1990.258.5.f1237 |
| Popis: | Albuminuria (UAlbV) can be reduced by converting-enzyme inhibitors (CEI), but the hormonal mechanism responsible for this effect has not previously been defined. Since CEI increase kinin activity as well as reduce angiotensin II (ANG II) activity, experiments were performed to determine the effect of isolated alterations in kinin and ANG II metabolism on UAlbV in rats with passive Heymann pephritis. Phosphoramidon was used to potentiate kinin activity without altering ANG II synthesis. Aprotinin was utilized in combination with the CEI, enalapril, to prevent the increase in kinin activity caused by CEI. UAlbV and the fractional renal clearance of albumin (FCAlb) decreased significantly after either phosphoramidon or enalapril, although only enalapril reduced blood pressure. Glomerular filtration rate (GFR) was not affected by either drug. Phosphoramidon did not affect plasma renin activity (PRA) or the pressor response to angiotensin I (ANG I), indicating that ANG II synthesis was not altered. Aprotinin prevented the reduction in UAlbV and FCAlb produced by CEI but not the hypotension, elevated PRA, or ANG I pressor blockade produced by CEI. Aprotinin alone had no effect on UAlbV, GFR, PRA, or blood pressure. UAlbV can be reduced by increasing kinin activity by a mechanism that is not dependent on suppression of ANG II activity or reduction in GFR or blood pressure. CEI may reduce proteinuria as a result of their action on the kallikrein-kinin system rather than on the renin-angiotensin system. |
| Databáze: | OpenAIRE |
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