Change in the level of nfkbp65 gene expression in the myocardium and kidneys of wistar rats and spontaneously hypertensive rats (shr) that received diet rich in nacl

The notions that a diet rich in common salt is an independent myocardium remodelling determinant, not associated with blood pressure (BP) increase, attract interest at present time. Possibly, this mechanism is implemented due to activation of proliferative, proliferative, proinflammatory and profibrotic cytokines, the signal pathways of which are controlled by hanges in expression of the line of nuclear transcription factors. Study the impact of diets with high and normal common salt content at BP and the level of expression of nuclear transcription factor κB (NFκB) in the myocardium and kidneys of normotensive Wistar rats and spontaneously hypertensive rats (SHR). Wistar and SHR rats, that received the diet with normal (0.34%) or high (8.0%) NaCl content for 2 months, were studied. The groups included eight animals each. In the end of the experiment, the systolic BP value and the left ventricular muscle mass indices (LVMMI) were estimated in rats. After removal from the experiment, the relative level of NFkBp65 gene expression in the myocardium and kidneys was determined. Total RNA was isolated with the phenol chloroform method. The preparation of cDNA was carried out by reverse transcription reaction with the use of reverse transcriptase M-MLV. Two separate reactions for NFkBp65 gene and GAPDH gene, respectively, were placed for each sample. The reaction mixture with the intercalating dye SYBRGRЕЕN was used for PCR analysis. Calculation of the relative level of NFkB gene expression was carried out under the semi-quantitative protocol by 2–ΔΔΡt method. Results are presented as mean ± SD. At this experiment term, the diet rich in salts caused no significant BP growth in Wistar rats (8 % NaCl–135.0 ± 5.0 mm Hg, 0.34% NaCl–130.0 ± 5.0 mm Hg, P > .05). In SHR rats, that received diet with 8 % NaCl content, the BP level (190 ± 10 mm Hg) also had no significant changes compared to the animals that administered 0.34% NaCl (190 ± 10 mm Hg, P > .05). However, despite the BP growth absence, against the background of the high salt diet, the increase of LVMMI (P < .01) and distinct changes in the NFκB gene expression level I the kidneys and myocardium were determined both in Wistar rats and in SHR rats. The NFkB gene expression level in myocardial tissue of Wistar rats with 8 % salt consumption was 3.4 times higher, and in renal tissue, 27.4 times higher than in animals, that received 0.34% of salt. It appeared to be 33 times higher in the myocardium tissue of the SHR rats that received feed rich in NaCl, and 12 times higher in renal tissue versus the rats that received the diet with normal salt content. High salt content in the diet is not always accompanied by BP growth; however, it causes activation of NFκB-associated signal pathways both in the myocardium and in kidneys of rats from various genetic lines. Possibly, it is accompanied by growth in expression of NFκB-associated proliferative, proinflammatory and profibrotic cytokines.