Premium
EFFECT OF HIGH SALT INTAKE ON LOCAL RENIN–ANGIOTENSIN SYSTEM AND VENTRICULAR DYSFUNCTION FOLLOWING MYOCARDIAL INFARCTION IN RATS
Author(s) -
De Resende Micheline M,
Mill José G
Publication year - 2007
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.2007.04556.x
Subject(s) - medicine , endocrinology , renin–angiotensin system , myocardial infarction , angiotensin ii , cardiac function curve , plasma renin activity , renal function , kidney , receptor , cardiology , heart failure , blood pressure
SUMMARY1 This study was performed to evaluate the effect of chronic high salt intake on local cardiac and renal components of the renin–angiotensin system (RAS) and its impact on cardiac remodelling and function after myocardial infarction (MI). 2 Rats submitted to coronary artery ligation to produce MI or sham operation (SO) were randomized to receive 1% NaCl solution or tap water as drinking water for 4 weeks. Plasma renin activity (PRA) and angiotensin‐converting enzyme (ACE) activity were quantified. Tissue angiotensin (Ang) II and ACE activity were determined by ELISA and a fluorimetric assay, respectively. Renal and cardiac AT 1 and AT 2 receptor protein levels were quantified by western blot. 3 Independent of the lower PRA levels, MI promoted a significant increase in the left ventricular/bodyweight ratio and impaired cardiac function. The cardiac RAS was activated after MI with a significant increase in ACE activity, AngII and AT 1 receptor levels. The RAS was slightly attenuated under high‐salt conditions. 4 Interestingly, high salt intake increased the expression of the AT 2 receptor by approximately twofold in the kidney of MI rats compared with the SO control group. Because of its natriuretic effect, the AT 2 receptor may counterbalance the salt overload and prevent the additional impairment of cardiac function. 5 The present study indicates that 4 weeks after MI, high salt intake did not further increase cardiac hypertrophy or further impair cardiac function in MI rats. A chronic increase in salt intake significantly suppressed PRA, but did not prevent activation of the local RAS or the progression of cardiac remodelling and left ventricular dysfunction caused by MI. 6 The present results show that inhibition of systemic renin production with salt overload does not affect ventricular remodelling after MI in rats. This suggests that local activation of the RAS in the heart, which was not suppressed by salt overload, exerts a predominant role for local adaptations of the heart after MI.