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High-sodium intake aggravates myocardial injuries induced by aldosterone via oxidative stress in Sprague-Dawley rats
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High-sodium intake aggravates myocardial injuries induced by aldosterone via oxidative stress in Sprague-Dawley rats
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High-sodium intake aggravates myocardial injuries induced by aldosterone via oxidative stress in Sprague-Dawley rats
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Journal Article
High-sodium intake aggravates myocardial injuries induced by aldosterone via oxidative stress in Sprague-Dawley rats
2012
Overview
Aim： To evaluate the effects of aldosterone with or without high sodium intake on blood pressure, myocardial structure and left ven- tricular function in rats, and to investigate the mechanisms underlying the effects. Methods： Eight-week-old male Sprague-Dawley rats were randomly divided into 3 groups： （1） control （CON） group fed a normal sodium diet, （2） aldosterone （ALD） group receiving aldosterone infusion and a normal sodium diet, and （3） high sodium plus aldosterone （HS- ALD） group receiving 1% NaCI diet in conjunction with aldosterone infusion. Aldosterone was administered through continuously sub- cutaneous infusion with osmotic minipump at the rate of 0.75 pg/h for 8 weeks. The myocardium structure was observed using transt- horacic echocardiography and transmission electron microscopy. The collagen deposition in left ventricle was evaluated with Masson＇s trichrome staining. The expression of IL-18, p22phox, and p47phox proteins was examined using Western blot analysis. Results： The systolic blood pressure in the ALD and HS-ALD groups was significantly higher than that in the CON group after 2-week treatment. But the blood pressure showed no significant difference between the HS-ALD and ALD groups. The left ventricular hyper- trophy, myocardial collagen deposition and oxidative stress were predominantly found in the HS-ALD and ALD group. Furthermore, the breakdown of myocardial structure and oxidative stress were more apparent in the HS-ALD group as compared with tho~e in the ALD group. Conclusion： Long-term infusion of aldosterone results in hypertension and profibrotic cardiovascular responsesin rats fed a normal sodium diet, which were mediated by oxidative stress. High-sodium intake could aggravate myocardial injuries induced by aldosterone.
