PROGRESSION OF GLOMERULOSCLEROSIS, RENAL HYPERTROPHY, AND AN INCREASED EXPRESSION OF FIBRONECTIN IN THE RENAL-CORTEX ASSOCIATED WITH AGING AND SALT-INDUCED HYPERTENSION IN DAHL SALT-SENSITIVE RATS

Citation
T. Takizawa et al., PROGRESSION OF GLOMERULOSCLEROSIS, RENAL HYPERTROPHY, AND AN INCREASED EXPRESSION OF FIBRONECTIN IN THE RENAL-CORTEX ASSOCIATED WITH AGING AND SALT-INDUCED HYPERTENSION IN DAHL SALT-SENSITIVE RATS, Life sciences, 61(16), 1997, pp. 1553-1558
Citations number
24
Categorie Soggetti
Biology,"Medicine, Research & Experimental","Pharmacology & Pharmacy
Journal title
ISSN journal
00243205
Volume
61
Issue
16
Year of publication
1997
Pages
1553 - 1558
Database
ISI
SICI code
0024-3205(1997)61:16<1553:POGRHA>2.0.ZU;2-3
Abstract
Aging and hypertension are known to be closely related with the pathog enesis and development of glomerulosclerosis. In this study, we examin ed the time course changes in the glomerulus associated with salt-indu ced hypertension using the inbred Dahl salt-sensitive rats. For this p urpose, 5-week-old Dahl salt-sensitive rats (n=36) were fed either 4 % NaCl diet (n=18) or 0.3 % NaCl diet (n=18) up to 17 weeks of age. The high salt diet caused a dramatic increase in systolic blood pressure and also a dramatic renal hypertrophy as shown by a significant increa se in the kidney weight. Histological examination revealed an age-depe ndent progression of glomerulosclerosis as documented by a quantitativ e scoring. This age-dependent progression was further accelerated by t he co-existence of salt-induced hypertension in the high salt diet gro up. Northern blot analysis revealed an increase in the steady state mR NA levels of fibronectin, an important component of mesangial matrices , in the renal cortex, but not in the renal medulla, only in salt-load ed Dahl salt-sensitive rats. These findings indicate that salt-induced hypertension accelerates the age-dependent progression of glomerulosc lerosis in Dahl salt-sensitive rats, and fibronectin may play a role i n the pathogenesis, development, and progression of glomerulosclerosis associated with salt-induced hypertension.