Dopamine and angiotensin as renal counterregulatory systems controlling sodium balance

To review the recent evidence demonstrating how the renal dopaminergic and angiotensin systems control renal electrolyte balance through various receptor-mediated pathways with counterregulatory interactions.

Stimulation of the renal rennin-angiotensin system results in increased sodium reabsorption, whereas the opposite is true for stimulation of the renal dopaminergic system. An underactive renal dopaminergic system has been associated with increased sodium reabsorption and hypertension. Recent findings indicate novel cell surface receptor-mediated mechanisms by which these two renal endocrine systems directly counterregulate each other. Each of the dopamine receptors (D1R through D5R) have been implicated in dopamine-mediated natriuresis, in addition to counterregulating the angiotensin type 1 R. Dopamine D1-like (D1R and D5R) stimulation has also been found to induce an AT2 receptor- dependent natriuresis. Recently, it has also been discovered that reactive oxygen species can play a role in inactivating the D1 receptor and activating the angiotensin type 1 R.

Current therapeutic interventions for hypertension predominantly involve correction of an overactive rennin-angiotensin aldosterone system. Recent evidence suggests that stimulation of the renal dopaminergic system and possibly activation of AT2 receptors, as well as decreasing reactive oxygen species, may provide additional therapeutic approaches.