| Autor: |
Franco M, Tapia E, Gabbai F, Cermeño JL, Calleja C, Pérez JM, Barrios R, Torres G, González FJ, Alvarado JA, et. al. |
| Jazyk: |
Spanish; Castilian |
| Zdroj: |
Archivos del Instituto de Cardiologia de Mexico [Arch Inst Cardiol Mex] 1986 Jan-Feb; Vol. 56 (1), pp. 13-24. |
| Abstrakt: |
To characterize the decrease in glomerular permeability that occurs in contralateral kidney of renovascular hypertension, glomerular hemodynamics were studied in Goldblatt hypertensive and normotensive control rats. The effects of converting enzyme inhibition (captopril) and renal vasodilatation induced with hyperoncotic plasma were evaluated: in addition, glomerular morphometry was performed. In hypertension, glomerular capillary pressure was increased, ultrafiltration coefficient was decreased, single-nephron filtration rate was normal and afferent resistance was elevated. Captopril rose glomerular filtration rate only in normotensive rats, but ultrafiltration coefficient increased in both groups. Hyperoncotic plasma induced a 98% increment in filtration rate and ultrafiltration coefficient rose by 48% in normotensive group. In hypertensive rats, filtration rate increased only 15% and ultrafiltration coefficient diminished 6%, morphometric studies showed dilatation of capillary loops and a larger glomerular volume. Similar response to captopril in both groups of rats suggest that the reduction in ultrafiltration coefficient in hypertension is not dependent of angiotensin; lack of response to hyperoncotic plasma suggests that it could be produced by structural changes in capillary wall that diminish hydraulic permeability since the larger glomerular volume indicates a greater area for filtration. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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