Arterial hipertension induced by saline overload: role of chloride anion

KOUYOUMDZIAN NM; ROBBESAUL GD; PRINCE PD; KIM G; PANDOLFO M; GALLEANO M; CHOI MR

Mar del Plata

Congreso; LXIV Reunión Anual de la Sociedad Argentina de Investigación Clínica (SAIC); 2019

Sociedad Argentina de Investigación Clínica

A chronicsaline (as sodium chloride) overload (SO) in the diet induces a renalinflammatory response and oxidative stress, which lead to the development ofhypertension. The aim ofthis work was to demonstrate the hypothesis that chloride anion (Cl-),besides sodium cation (Na+), is involved in these inflammatory andoxidative responses. These alterations might be diminished if Cl- isreplaced by other anion (like citrate), or if Na+ is replaced byother cations.Male Wistarrats were randomly divided into four experimental groups (n=8): control (C);SO (NaCl 8% W/W); high Na+ without Cl- (Na:Na3C6H5O711,8%); high Cl- without Na+ (Cl: CaCl23,80%; KCl 3,06% and MgCl2 1,30%). After three weeks, systolic bloodpressure (SBP) was measured, and rats were housed in metabolic cages in order tocollect 24-hour urine to assess renal function. Oxidative stress parameterswere measured in renal cortex: TBARS production andantioxidant enzymes activitiesand expression:superoxide dismutase (SOD), catalase (CAT) and glutathioneperoxidase (GPx). In all the experimentalgroups we observed a significant increase of diuresis (*p<0,05 versus C) whileSBP was increased only in those rats fed with Cl- (mmHg, C:125±9;NaCl:164±8*; Na:133±4; Cl:152±7*). These changes wereaccompanied by an increase in TBARS production in renal cortex (mol TBARS/mgprotein) (x10^12): C:1,30±0,10; NaCl:1,82±0,18*; Na:2,01±0,32*;Cl:1,91±0,34*. No changes were observed on the activity or expression ofSOD and CAT. Despite the fact that GPx expression was unaltered, the enzyme activitywas increased in those groups with Cl- (μmol GSSG/mgprotein.min, C:1,34±0,14; NaCl:2,31±0,37*; Na:1,30±0,14; Cl:2,77±0,52*).Theseresults suggest a relevant role of Cl- in the development ofhypertension, independently on Na+. Saline overload, and both ionsseparately, induced lipid oxidative damage. Nevertheless, only Cl- saltdiets produced an increase in GPx activity, resulting in a high prooxidantstate in kidney.