The chloride anion is neccesary for the development of arterial hypertension and renal damage induced by salt

RUDI, MARÍA JULIETA; KOUYOUMDZIAN NM; KIM G; GALLEANO M; FERNÁNDEZ BE; PUYÓ AM; CHOI MR

Congreso; LXVI Reunión Anual de la Sociedad Argentina de Investigación Clínica (SAIC); 2021

Sociedad Argentina de Investigación Clínica (SAIC)

The excessive consumption of sodium chloride is a risk factor forarterial hypertension (AH) and induces a renal inflammatory and oxidativeresponse. The contribution of the chloride anion (Cl-) to thesedeleterious effects is unknown.The objective was to evaluate whether Cl-, independent of sodium(Na+), would be involved in the renal and oxidative inflammatory responseand in the development of AH.Male Wistar rats were divided in four groups (n=8/group) and fedwith different diets (3 weeks): control (C); high sodium chloride (NaCl8%); high Na+ without Cl- (Na3C6H5O7 11.8%); high Cl- without Na+(CaCl2 3.80%; KCl 3.06%; MgCl2 1.30%). Systolic blood pressure(SBP), renal function and oxidative parameters in renal cortex weredetermined: activity and expression (by WB) of enzymes superoxidedismutase (SOD), catalase (CAT) and glutathione peroxidase(GPx). We also determine chloride channels expression (CLCN5and CLCNKa) as key transporters to elicit this process.Results: SBP increased in NaCl and Cl- groups (p<0.05). TBARSproduction increased in all three diets, without changes in the activityand expression of SOD and CAT, while the activity of GPx increasedonly in Cl- group (p<0.05). Additionally, compared with Cgroup, NFkB expression in the kidney was increased in NaCl and Clgroups(p<0.05), while CLCNKa expression increased in Cl- groupand CLCN5 decreased in NaCl group.Conclusion: Cl- contributes, at least in part, in the development ofAH induced by NaCl overload, and diets with a high chloride contentwould be associated with a higher prooxidant state in kidney thanonly sodium salt diets. The role of chloride transporters as mediatorsof oxidative damage or for the development of AH remains tobe elucidated.