Selective role of dopamine in the natriuresis produced by iso-osmotic saline infusion.

Abstract

Endogenous dopamine (DA) selectively contributes to the natriuresis (UNaV) produced by infusion and dietary consumption of sodium chloride. The present study in anesthetized rats determined whether DA has a role in the natriuresis produced by small (2.0 +/- 0.11% increase in body weight) and large (17.9 +/- 0.58% increase in body weight) increments in extracellular fluid volume with iso-osmotic saline. Small volume expansion increased urine flow (V) by 59 +/- 15%, UNaV by 155 +/- 31%, and dopamine excretion by 25 +/- 9%. DA1-receptor blockade with SCH 23390 (SCH, 1.0 microgram/kg/min), attenuated the natriuresis; an increase in UNaV of only 69 +/- 15%. Large volume expansion increased V by 1,026 +/- 215% and UNaV by 2,735 +/- 899%, without affecting dopamine excretion. Increments in V and UNaV were unaffected by increasing doses of SCH (1.0 microgram/kg/min; 10 micrograms/kg/min; and 50 micrograms/kg bolus, followed by 10 micrograms/kg/min). Adequacy of DA1-receptor blockade was demonstrated by the fact that SCH (1.0 microgram/kg/min) attenuated the natriuresis produced by the DA1-receptor agonist, fenoldopam (0.1 micrograms/kg/min ia). We conclude that endogenous DA contributes to the natriuresis produced by small, but not large, increases in extracellular fluid volume with iso-osmotic saline.