The natriuretic response to dopamine DA1 agonist requires endogenous activation of dopamine DA2 receptors

Abstract

The kidneys act as an endocrine and paracrine organ. Dopamine produced in the kidney acts as a natriuretic hormone by inhibiting tubular NA+K+-ATPase activity. Previous in vitro studies have shown that NA+K+-ATPase activity in the proximal tubule is inhibited by a synergistic action of dopamine 1 (DA1) and dopamine 2 (DA2) receptors. This in vivo study performed in adult rats, investigates whether the natriuretic response to DA requires a synergistic action of DA1 and DA2 receptors. Fenoldopam, a DA1 agonist significantly increases the sodium excretion but there is no increase in urinary sodium excretion when the DA1 agonist is given together with a DA2 antagonist. Neither DA1 nor DA2 antagonist had any influence on the sodium excretion. The natriuretic response to fenoldopam was also significant attenuated after the administration of benserazide, which inhibits aromatic acid decarboxylase and thereby suppresses the endogenous production of dopamine. The dose used of dopamine and fenoldopam 1.5 µg/kg b.w./Min for both drugs did not affect the mean arterial pressure or the glomerular filtration rate. In conclusion, the natriuretic effect appears to be constitutively activated by endogenous dopamine.