Hemodynamic and Natriuretic Responses to Intravenous Infusion of Dopamine in Patients with Essential Hypertension

Abstract

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 μg/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 ΔUNaV and ΔFENa or ΔFEP, and between ΔFENa and ΔFEP, while no significant relation was observed between ΔUNaV and ΔCcr, ΔMAP or MAP before dopamine infusion. A significant inverse correlation between supine PRA before dopamine infusion and ΔFENa or ΔFEP and a positive correlation between age and ΔFENa or ΔFEP were also observed in these patients. The changes in UNaV positively correlated with ΔFENa and ΔFEP in both low renin (group L) and normal renin EHT (group N) and with ΔCcr in group N but not in group L. The mean values of ΔFENa, ΔFEP and ΔFEK 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 disturbance of water-sodium metabolism, at least in part, in the pathophysiological mechanism in EHT, particularly in group L. © 1982, The Japanese Circulation Society. All rights reserved.