To explore whether an altered metabolic pathway of
dihydroxyphenylalanine (
DOPA) may be related to some previously observed
dopamine abnormalities in borderline
hypertension, we measured basal and
DOPA-induced (500 mg orally) changes in blood pressure and pulse rate as well as in three hourly plasma and urine samples. We found that borderline hypertensive patients compared with controls 1) showed a higher baseline urinary excretion of
methoxytyramine, a marker of exocytotic
dopamine release, with a greater
DOPA-induced decrease of systolic blood pressure without reflex
tachycardia; 2) had in response to
DOPA a blunted plasma
DOPA and free
dopamine increase but an accentuated plasma
dopamine sulfate and urinary
DOPAC excretion; and 3) eliminated comparable quantities of
dopamine in urine despite a lower rise in the glomerular
DOPA load. Furthermore, although
DOPA elicited natriuresis in both groups, its effect was greater in borderline hypertensive patients, who lacked the urinary
sodium correlation with urinary
dopamine excretion seen in control subjects. These data are compatible with increased basal exocytotic
dopamine release and accelerated neuronal and renal (extraneuronal)
dopamine generation from administered
DOPA in borderline
hypertension. The
DOPA-induced hypernatriuresis exceeding augmented
dopamine in borderline hypertensive patients, contrasting with the urinary
sodium and
dopamine correlation in control subjects, suggests that
DOPA induced an additional natriuresis in borderline hypertensive patients by a decrease in renal sympathetic tone because of its central inhibition of sympathetic outflow, which also may account for the absence of reflex
tachycardia.