Myocardial remodeling in wistar rats with renal dysfunction fed a high-salt diet

Abstract

BACKGROUND. Dietary adjustment is an important point in the treatment of chronic kidney disease (CKD). However, at present, the effect of a diet with a high NaCl content on the state of the cardiovascular system in patients with early stages of CKD has not been sufficiently studied.The AIM: to evaluate blood pressure levels and changes in the myocardium of Wistar rats with early stage renal dysfunction fed a high-salt diet for a long time.MATERIALS AND METHODS: The study was performed on male Wistar rats. The control group consisted of sham-operated animals (LO-group), receiving a standard diet (0.34 % NaCl), the second – rats subjected to resection of ¾ of the kidney parenchyma, receiving a standard diet (NE-group), the third – rats, subjected to ¾ NE, receiving high sodium diet (4  % NaCl, NE+HSD). After 4 months, the rats were assessed for blood pressure (BP), levels of urea, creatinine, sodium in the blood serum, daily diuresis, albumin content in the urine, myocardial mass index (IMM) and left ventricular myocardial mass index (IMLV), and a histological examination of the myocardium was performed.RESULTS: In rats with kidney dysfunction, an increase in blood pressure was detected, most pronounced in the NE+HSD group. In rats of this group, albumin excretion, connective tissue volume, arterial diameter, thickness of the adventitia and media of myocardial vessels increased relative to the indicators of rats with NE receiving a standard diet. IMLV in NE+HSD rats was higher by 16.4 %, and IMM by 10.9 % than in animals with NE on a standard diet. The groups with NE did not differ from each other in the content of urea and creatinine in the blood serum, although these indicators were higher than in LO animals. There were no differences between groups in serum sodium levels.CONCLUSION: Prolonged consumption of a diet with a high content of table salt contributes to the development of the initial stages of CKD in Wistar rats, promotes blood pressure growth and myocardial remodeling, manifested primarily in the progression of cardiomyocyte hypertrophy and myocardial fibrosis.