INVESTIGADORES
PERAL Maria De Los Angeles
artículos
Título:
STRUCTURAL CHANGES IN RENAL TISSUES INDUCED BY AORTIC COARTACTION
Autor/es:
MARIA DE LOS ANGELES PERAL; COVIELLO, A; HECTOR, R.; RODRIGO, M.; JOO TURONI C,
Revista:
CLINICAL AND EXPERIMENTAL HYPERTENSION
Editorial:
Editorial Marcel Dekker Inc
Referencias:
Lugar: Nueva York , USA; Año: 2001 vol. 23 p. 506 - 511
ISSN:
1064-1963
Resumen:
The objective of present work was the study of structural alterations in renal tissue, identifying the morphological and histological changes in the non ischemic kidney (NIK) and their possible significance in aortic coarctation-hypertensive rats (HR).After 7-14 days of complete ligature of the aorta between both renal arteries mean arterial blood pressure (MAP) was higher (p<0.01) in HR compared with sham operated rats (SR) (183,6 ± 6,8 n=6 versus 110,5 ± 3,0 mm Hg, n=6). Kidneys from each group were obtained (ischemic kidney, IK and NIK) for morphological and histological evaluation. SR did not presented differences between both kidneys In HR hypertrophy of NIK occured with a significant increase of weight p<0.01, thickness p<0.01 and width p<0.05, whereas the IK did not presented regression in size as compared with SR. The ratio IK/NIK in HR was decreased by 22% (p<0.01), 11 % (p<0.05) and 18,4 % (p<0.05) for the weight, thickness and width respectively without difference in length. Renal mass index (RMI): kidney weight/body weight was greater in HR (p<0.01).These results are in agreement with microscopic studies in which it was observed that IK presented signs of ischemia, subtotal necrosis, focal hemorrhage and polymorphonuclear infiltrate whereas in the NIK it was found glomerulosclerosis, mesangial proliferation, tubular dilatation and remodeling in preglomerular vessels. Stereological study of afferent arterioles in NIK showed hypertrophy with an increase in the ratio wall/lumen with a similar lumen but a significantly greater wall thickness as compared with SR vessels. The fact that a greater RMI was found in HR would indicate that the NIK may play a compensatory role in this angiotensin II-dependent model of hypertension.