Salt Induces Myocardial and Renal Fibrosis in Normotensive and Hypertensive Rats

Yu, Henry C.; Burrell, Louise M.; Black, M. Jane; Wu, Linlin; Dilley, Rodney J.; Cooper, Mark E.; Johnston, Colin I.

doi:10.1161/01.cir.98.23.2621

Cited by 320 publications

(283 citation statements)

References 25 publications

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Section: Discussionmentioning

confidence: 99%

“…The prohypertrophic cardiac and vascular effects of high dietary sodium, independent of blood pressure, is well documented when the amount of sodium, as well as the duration of exposure, are large enough (10,13,14,19,23). At variance with Wistar (9), Wistar Kyoto, and spontaneously hypertensive rats (23), no clear enhancement of fibrosis was detected in the Sprague-Dawley rats, despite a longer duration of high sodium feeding. Although the circulating renin activity drastically fell during high sodium intake, an enhanced activity and expression of the renin-angiotensin system were reported in cardiac (8,19) and vascular tissue (12).…”

Section: Discussionmentioning

confidence: 99%

“…On the contrary, a low-sodium diet entirely prevented the cardiac hypertrophy associated with chronic infusion of ANG II (14), thus suggesting a role for tissue ANG II in the response of the cardiovascular system to salt intake changes. In addition, the stimulation of cardiac expression of TGF-␤ 1 , directly by high dietary sodium (23) or through ANG II (7) or endothelin (20) may underlie the hypertrophic and fibrotic changes observed in rats.…”

Section: Discussionmentioning

confidence: 99%

“…Reversal of cardiac hypertrophy was achieved by 6 wk on a low-sodium diet in 2-kidney, one-clip hypertensive rats (17). Administration of a diet containing 8% sodium chloride for more than 4 wk was associated with the development of left ventricular hypertrophy, cardiac fibrosis, and an increase in collagen content (10,23).Because an increase in systemic pressure associated with high sodium was not consistently observed, it was suggested that a direct effect of sodium may underlie the increased sensitivity of target organs to blood pressure. Interestingly, in a cohort of normotensive subjects and never-treated patients with essential hypertension, it was recently demonstrated that increasing dietary sodium (as estimated by 24-h natriuresis), enhanced the slope of the relationship between left ventricular mass index or albuminuria and systolic blood pressure (5).…”

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confidence: 99%

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Cardiorenal abnormalities associated with high sodium intake: correction by spironolactone in rats

Cordaillat

Rugale

Casellas

et al. 2005

American Journal of Physiology-Regulatory, Integrative and Comp

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Cordaillat, Magali, Caroline Rugale, Daniel Casellas, Albert Mimran, and Bernard Jover. Cardiorenal abnormalities associated with high sodium intake: correction by spironolactone in rats. Am J Physiol Regul Integr Comp Physiol 289: R1137-R1143, 2005. First published May 26, 2005; doi:10.1152/ajpregu.00154.2005.-Reversal by the mineralocorticoid receptor antagonist spironolactone on cardiac and renal abnormalities, associated with long-term (since weaning) administration of a high (2 and 8% NaCl chow, HS2 and HS8) sodium diet, was assessed in Sprague-Dawley rats. At the age of 5 mo, spironolactone (20 or 100 mg/kg, gavage) or placebo were given for 14 days to HS2 and HS8 rats. A group fed a regular diet (0.8% NaCl, NS) remained untreated. High sodium intake had no detectable effect on blood pressure; however, cardiac mass index and cross-sectional area of the carotid artery, as well as albuminuria, were increased only in the HS8 group compared with the control group on NS diet. In addition, a marked reduction in glomerular filtration rate (by 40%), associated with a nonproportional fall in renal plasma flow (thus resulting in a decrease in filtration fraction), was observed only in the HS8 group. No change in cardiac and renal fibrosis was detected. Production of the reactive oxygen species (ROS) by aortic tissue was increased in HS8 rats, whereas ROS production by the heart was unaffected. Only the high dose of spironolactone was effective, as it markedly reversed the cardiac hypertrophy and renal hypofiltration associated with the HS8 feeding. The changes were observed in the absence of any effect on systemic blood pressure and production of ROS. These observations favor aldosterone's role in the deleterious effects of marked and prolonged increases in sodium intake. spironolactone; renal function; reactive oxygen species; cardiac hypertrophy IN ADDITION TO ITS WIDELY debated effect on blood pressure, chronic variation of sodium intake has been reported to modulate the cardiovascular morphology in human and experimental models. In animal studies, dietary sodium restriction has been shown to prevent the development of cardiac hypertrophy in renovascular (13) and ANG II-induced hypertension (14), independently of blood pressure. Reversal of cardiac hypertrophy was achieved by 6 wk on a low-sodium diet in 2-kidney, one-clip hypertensive rats (17). Administration of a diet containing 8% sodium chloride for more than 4 wk was associated with the development of left ventricular hypertrophy, cardiac fibrosis, and an increase in collagen content (10,23).Because an increase in systemic pressure associated with high sodium was not consistently observed, it was suggested that a direct effect of sodium may underlie the increased sensitivity of target organs to blood pressure. Interestingly, in a cohort of normotensive subjects and never-treated patients with essential hypertension, it was recently demonstrated that increasing dietary sodium (as estimated by 24-h natriuresis), enhanced the slope of the relationship between...

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