ACUTE INFUSION OF ANGIOTENSIN II REGULATES ORGANIC CATION TRANSPORTERS FUNCTION IN THE KIDNEY: ITS IMPACT ON RENAL DOPAMINERGIC SYSTEM AND SODIUM EXCRETION

KOUYOUMDZIAN NM; RUKAVINA MIKUSIC NL; ROBBESAUL GD; GORZALCZANY S; CARRANZA A; TRIDA VA; FERNÁNDEZ BE; CHOI MR

HYPERTENSION RESEARCH

NATURE PUBLISHING GROUP

Lugar: Londres; Año: 2021 vol. 44 p. 286 - 298

0916-9636

A close relationship between angiotensin II (ANG II) and renal dopaminergic system(RDS) has been reported. Our aim was to study whether renal dopamine and ANG II are able tointeract to modify renal sodium handling and elucidate the mechanism implied. Anesthetizedmale Sprague Dawley rats were used in the experiments. ANG II, exogenous dopamine anddecynium-22 (or D-22, an isocyanine that specifically blocks electrogenic organic cationtransporters named OCTs), were infused in vivo for 120 minutes. We determined renal andhemodynamic parameters, renal Na+,K+?ATPase, OCTs activity and urinary dopamineconcentration. We also evaluated D1 Receptor, electroneutral organic cation transporters(OCTNs) and OCTs expression. ANG II decreased renal excretion of sodium in the presence ofexogenous dopamine, increased Na+,K+?ATPase activity and decreased urinary dopamineconcentration. All these effects were prevented by D-22. The infusion of ANG II did not affectthe expression of D1 Receptor, OCTs and OCTNs. However, OCTs activity was diminished by thepresence of ANG II. Although ANG II did not alter the expression of D1 Receptor, OCTs and OCTNsin renal tissues, it modified OCTs activity and thereby decreased urinary dopamineconcentration, showing a novel mechanism by which ANG II decreases dopamine transport andits availability in the tubular lumen to stimulate D1 Receptor. This study demonstrates arelationship between ANG II and dopamine to counteract its effects on sodium excretion.