Hemodynamic and natriuretic responses to intravenous infusion of dopamine in patients with essential hypertension.

In order to clarify the role of dopamine on the pathophysiology of essential hypertension, mean arterial pressure (MAP), heart rate (HR), urine volume (UV), urinary sodium excretion (UNaV), endogenous creatinine clearance (Ccr), fractional excretions of sodium (FENa), inorganic phosphorus (FEP) and potassium (FEK), plasma renin activity (PRA), plasma aldosterone concentration (PAC) and plasma noradrenaline concentration (PNA) were measured before and after intravenous infusion of dopamine (3 micrograms/kg/min, 60 min) in normotensive (NT) and essential hypertensive subjects (EHT). Following dopamine infusion, a significant decrease of MAP and an increase of HR were observed in EHT but not in NT. UV, UNaV, Ccr, FENa, FEP and FEK increased significantly in both NT and EHT, and changes in these except for Ccr were significantly greater in EHT than in NT. In EHT, following dopamine infusion, PNA was clearly elevated, but no remarkable change was found in PRA and PAC. A significantly positive correlation was found between delta UNaV and delta FENa or delta FEP, and between delta FENa and delta FEP, while no significant relation was observed between delta UNaV and delta Ccr, delta MAP or MAP before dopamine infusion. A significant inverse correlation between supine PRA before dopamine infusion and delta FENa or delta FEP and a positive correlation between age and delta FENa or delta FEP were also observed in these patients. The changes in UNaV positively correlated with delta FENa and delta FEP in both low renin (group L) and normal renin EHT (group N) and with delta Ccr i group N but not in group L. The mean values of delta FENa, delta FEP and delta FEK were significantly higher in group L as compared with those in age-matched group N. These results suggest that, since the enhanced response to infused dopamine may reflect reduced dopaminergic activity, attenuation of renal dopaminergic activity might exist and be involved through a distribution of water-sodium metabolism, at least in part, in the pathophysiological mechanism in EHT, particularly in group L.