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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Salt-Induced Cardiac Hypertrophy and Interstitial Fibrosis Are Due to a Blood Pressure-Independent Mechanism in Wistar Rats

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Author(s):
Ferreira, Daniele N. [1] ; Katayama, Isis A. [1] ; Oliveira, Ivone B. [1] ; Rosa, Kaleizu T. [2] ; Furukawa, Luzia N. S. [1] ; Coelho, Michella S. [2] ; Casarini, Dulce E. [3] ; Heimann, Joel C. [1]
Total Authors: 8
Affiliation:
[1] Univ Sao Paulo, Lab Expt Hypertens, Sch Med, BR-01246903 Sao Paulo - Brazil
[2] Univ Sao Paulo, Inst Heart, Sch Med, BR-01246903 Sao Paulo - Brazil
[3] Univ Fed Sao Paulo, Div Nephrol, Dept Med, BR-04002390 Sao Paulo - Brazil
Total Affiliations: 3
Document type: Journal article
Source: Journal of Nutrition; v. 140, n. 10, p. 1742-1751, OCT 2010.
Web of Science Citations: 27
Abstract

High salt intake is a known cardiovascular risk factor and is associated with cardiac alterations. To better understand this effect, male Wistar rats were fed a normal (NSD: 1.3% NaCl), high 4 (HSD4: 4%), or high 8 (HSD8: 8%) salt diet from weaning until 18 wk of age. The HSD8 group was subdivided into HSD8, HSD8+HZ (15 mg.kg(-1).d(-1) hydralazine in the drinking water), and HSD8+LOS (20 mg.kg(-1).d(-1) losartan in the drinking water) groups. The cardiomyocyte diameter was greater in the HSD4 and HSD8 groups than in the HSD8+LOS and NSD groups. Interstitial fibrosis was greater in the HSD4 and HSD8 groups than in the HSD8+HZ and NSD groups. Hydralazine prevented high blood pressure (BP) and fibrosis, but not cardiomyocyte hypertrophy. Losartan prevented high BP and cardiomyocyte hypertrophy, but not fibrosis. Angiotensin II type 1 receptor (AT(1)) protein expression in both ventricles was greater in the HSD8 group than in the NSD group. Losartan, but not hydralazine, prevented this effect. Compared with the NSD group, the binding of an AT(1) conformation-specific antibody that recognizes the activated form of the receptor was lower in both ventricles in all other groups. Losartan further lowered the binding of the anti-AT(1) antibody in both ventricles compared with all other experimental groups. Angiotensin II was greater in both ventricles in all groups compared with the NSD group. Myocardial structural alterations in response to HSD are independent of the effect on BP. Salt-induced cardiomyocyte hypertrophy and interstitial fibrosis possibly are due to different mechanisms. Evidence from the present study suggests that salt-induced AT(1) receptor internalization is probably due to angiotensin II binding. J. Nutr. 140: 1742-1751, 2010. (AU)

FAPESP's process: 05/50053-7 - High salt intake: mechanisms of left ventricular hypertrophy development
Grantee:Daniele Nunes Ferreira
Support Opportunities: Scholarships in Brazil - Doctorate (Direct)