Relationship between Urinary Dopamine Production and Natriuresis after Acute Intravascular Volume Expansion with Sodium Chloride in Dogs*

Abstract

The role of renal production of dopamine in mediating the natriuretic response to acute vascular volume expansion was investigated. The effect of infusion of 0.9% saline (30 ml/kg·h) over 2 h on urine excretion of sodium and catecholamines, as well as other hemodynamic and renal function parameters, was examined in seven dogs during control and carbidopa (1 mg/kg every 8 h for 24 h before saline infusion) treatment periods. Acute vascular volume expansion with saline resulted in a rise (P < 0.01) in the renal excretion of dopamine and a depression (P < 0.01) in renal excretion of norepinephrine which paralleled the natriuretic response to saline infusion. Epinephrine excretion was not altered by saline infusion. Carbidopa treatment was not associated with changes in left ventricular filling pressure, arterial blood pressure, glomerular filtration rate, renal blood flow, renal excretion of norepinephrine or epinephrine. However, carbidopa eliminated the increase in renal production of dopamine and markedly attenuated the natriuretic response to saline infusion. Since carbidopa blocks tissue conversion of dopa to dopamine, it appears that renal production of dopamine is an important mechanism mediating the natriuretic response to acute volume expansion. (Endocrinology115: 2085–2090, 1984)