STRUCTURAL CHANGES IN THE KIDNEY INDUCED BY COARCTATION HYPERTENSION
| Autor: | María Peral de Bruno, Alfredo Coviello, Claudio M Joo Turoni, Héctor A. Reynoso, Rodrigo O Maranon |
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| Rok vydání: | 2001 |
| Předmět: |
Male
Pathology medicine.medical_specialty Physiology Urinary system Kidney Aortic Coarctation Losartan Rats Sprague-Dawley Renal Artery Text mining Heart Rate Rats Inbred SHR Renin–angiotensin system Internal Medicine Animals Medicine Histology Comparative skin and connective tissue diseases Antihypertensive Agents business.industry Vascular disease Body Weight Renal tissue Histology Organ Size General Medicine medicine.disease Rats Surgery Disease Models Animal medicine.anatomical_structure Hypertension sense organs Complication business |
| Zdroj: | Clinical and Experimental Hypertension. 23:501-511 |
| ISSN: | 1525-6006 1064-1963 |
| DOI: | 10.1081/ceh-100104241 |
| Popis: | We investigated structural alterations in renal tissue identifying the morphological and histological changes in the non-ischemic kidney (NIK) and their potential significance in aortic coarctation-hypertensive rats (HR). HR's mean arterial pressure (MAP) was higher compared with sham operated rats (SR). An oral 10 mg/kg/day losartan (LOS) dose diminished but not reverted MAP. Hypertrophy was noted in HR NIK's with significant weight increase (p0.01). The ratio IK/NIK in HR's decreased 22% (p0.01). LOS proved to cause no ischemic kidney (IK) modification nor did it revert NIK hypertrophy. NIK in HR's presented glomerulosclerosis, mesangial proliferation and arteriolar thickening reverted by LOS. The stereological study of afferent NIK arterioles showed hypertrophy and an increase in the wall/lumen ratio without lumen modification. LOS diminished wall thickness. LOS-induced decrease of NIK alterations might result from arteriosclerosis regression, the media/lumen ratio. glomerulosclerosis and mesangial proliferation dependent on angiotensin 11. |
| Databáze: | OpenAIRE |
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