Is chloride responsible for NaCl-renal acute inflammatory effect?

KOUYOUMDZIAN, NICOLÁS MARTÍN; CAO, GABRIEL; FERNÁNDEZ, BELISARIO ENRIQUE; ROBBESAUL GD; PANDOLFO, MARCELA; CHOI, MARCELO ROBERTO; SÁNCHEZ GELÓS DF; GORZALCZANY, SUSANA; GIARDINA, GRACIELA; ROSÓN, MARÍA INÉS

Congreso; Joint Meeting European Society of Hypertension; 2019

Introduction. NaCl and simple carbohydrates-rich diets induce tissue oxidative stress, overexpression of inflammatory cytokines and fibrotic molecules which lead to hypertension and damage of noble organs, including the kidney.Aim. The aim of this work was to demonstrate in vivo the contribution of chloride anion (Cl-) in the renal inflammatory process induced by an acute overload of NaCl and the contribution of an acute fructose (F) infusion as an enhancer of the deleterious effects of NaCl.Materials and procedures. Anesthetized male Wistar rats (n=5/group) were infused (0,05mL/min/2 hours) and randomized in the following groups: isotonic saline solution (Control group: ¬C), NaCl 1M, Na3Citr 0,33M, F 0,5M, NaCl+F, Na3Citr+F. Mean arterial pressure (MAP), urinary and plasmatic parameters, diuresis per minute, glomerular filtration rate (GFR), Na+ and Cl- tubular reabsorption (TRNa and TRCl) were determined. Tubular expression of inflammatory markers were determined by immunohistochemistry. Results were expressed as media ± SEM.Results. NaCl or F infused separately did not affect MAP, but their co-infusion increased MAP levels versus Control group (mmHg, C:77±2;NaCl+F:110±5,*p