HIGH URINARY DOPA AND LOW URINARY DOPAMINE-TO-DOPA RATIO IN SALT-SENSITIVE HYPERTENSION

Dopamine in urine is derived substantially from renal uptake and decarboxylation of 3,4-dihydroxyphenylalanine (dopa), and increases in excretion of dopa normally parallel increases in excretion of dopamine during salt loading. Since patients with salt-sensitive hypertension may have decreased urinary excretion of dopamine during dietary salt loading, the present study was designed to evaluate the response of dopa to salt loading. Sixteen inpatients with normal-renin essential hypertension ate a constant metabolic diet containing 9 mmol/day sodium for-7 days, followed by the same diet but containing 249 mmol/day sodium for 7 days. Salt sensitivity was defined as an increase in mean arterial pressure of 8 mm Hg between the diets; on this basis, nine patients were salt-sensitive and seven, salt-resistant. The rate of urinary dopa excretion was significantly higher in the salt-sensitive patients throughout the study (mean rates 132 +/- 13 nmol/day in the salt-sensitive group and 78 +/- 9 nmol/day in the salt-resistant group for the 14 days of observation, p < 0.01). When dietary sodium intake was increased to 249 mmol/day, urinary dopa excretion increased significantly more in salt-sensitive patients than salt-resistant patients. At the end of the high salt diet, dopamine excretion was significantly attenuated in the salt-sensitive patients, despite higher rates of dopa excretion. Thus, the urinary ratio of dopamine to dopa was decreased in salt-sensitive patients, regardless of salt intake. Among individual patients, cumulative sodium retention during the first 3 days of salt loading was unrelated to the magnitude of the pressor response; however, the dopa excretion rate was positively correlated with the magnitude of the pressor response (r = 0.62, p = 0.015). The results suggest that salt-sensitive patients have decreased renal uptake or decarboxylation of dopa and that this deficiency is associated with enhanced delivery of dopa to renal uptake sites during dietary salt loading. A high rate of urinary excretion of dopa and a low urinary dopamine/dopa ratio appear to be markers of salt-sensitive hypertension in humans.