Low-dose Dopamine Infusion Research Articles

Effect of low-dose dopamine on serum concentrations of prolactin in critically ill patients

Dopamine is a naturally occurring catecholamine with actions in the central nervous system and endocrine systems, including inhibition of prolactin release from the pituitary gland. Prolactin secretion has been shown to be increased in response to physiological stress, while hypoprolactinaemia is associated with a reduction in the cellular immune response. We have investigated the effects of low-dose infusion of dopamine 2.5 micrograms kg-1 min-1 on serum concentrations of prolactin in critically ill patients. Six hours after commencing the dopamine infusion, mean serum prolactin concentration had decreased from 746.95 to 128.9 mu. litre-1 (normal range 84-488 mu. litre-1). This represented a mean reduction of 79.2%, with 35% of patients exhibiting a subnormal concentration while receiving dopamine. This reduction was reversed after cessation of dopamine and reproducible on re-institution. This suppression of the release of dopamine may be a detrimental side effect of low-dose dopamine infusion in critically ill patients.

Dopamine—sodium relationship in Type 2 diabetic patients

Diabetes mellitus is known to be associated with sodium retention. The aim of the present paper was to investigate the possible role of the renal dopaminergic system in the disturbed sodium homeostasis of Type 2 diabetic patients. The urinary dopamine excretion, which represents the local kidney production, was lower in Type 2 diabetic patients as compared to controls and decreased in insulin treated patients as compared to patients treated without insulin. Urinary dopamine excretion correlated positively with sodium excretion in non-insulin treated patients and in controls, but not in insulin treated patients. In contrast to findings in healthy volunteers, an intravenous sodium load failed to increase the dopamine excretion in Type 2 diabetic patients, despite similar increments in sodium excretion. A low-dose dopamine infusion caused significantly lower natriuretic responses in insulin treated Type 2 diabetic patients as compared to controls, but not in non-insulin treated patients. These findings suggest that Type 2 diabetic patients display a derangement of the renal dopaminergic system, which is accentuated by insulin treatment.

High altitude-induced albuminuria in normal man is enhanced by infusion of low-dose dopamine.

Renal function and the urinary excretion rate of albumin (Ualb) at rest and during infusion of dopamine (3 micrograms kg-1 min-1) were investigated in eight normal volunteers at sea level and 48 h after a rapid, passive ascent to an altitude of 4350 m. Oxygen saturation decreased to 81% (77-85) (median with quartiles in parentheses) at high altitude. High altitude hypoxia increased Ualb from 3.2 micrograms min-1 (2.7-3.5) to 5.0 micrograms min-1 (3.3-6.6) (p < 0.05); increased mean arterial blood pressure from 80 mmHg (73-95) to 102 mmHg (96 108) (p < 0.01); decreased the effective renal plasma flow (ERPF) from 465 ml min-1 (412-503) to 410 ml min-1 (385-451) (p < 0.05), and increased the filtration fraction from 24% (22-27) to 28% (26-29) (p < 0.01). Glomerular filtration rate (GFR), and the renal clearances of lithium (CLi) and sodium (CNa) remained unchanged at high altitude. Dopamine increased ERPF, GFR, CLi, CNa, and decreased the filtration fraction in both environments. Infusion of dopamine further increased Ualb to 10.5 micrograms min-1 (5.5-64.8) (p < 0.05) at high altitude, but had no effect on Ualb at sea level. In conclusion, high altitude hypoxia per se increases the urinary excretion rate of albumin, which is further increased by the renal vasodilating drug dopamine. This effect of dopamine at high altitude may result from combined effects of the increase in renal plasma flow and a hypoxia-induced increase in the glomerular capillary permeability to albumin.

Reduced Renal Response to Low-Dose Dopamine Infusion in the Elderly

Increasing age is associated with a number of changes in renal function, including a diminished capacity to excrete salt and water loads and an increased susceptibility to acute renal failure. Dopamine is a renal autocoid important in diuresis and natriuresis and may also serve to protect against ischemic renal injury. The aim of this study was to assess the renal response to a low-dose dopamine infusion in healthy young vs elderly individuals. Five healthy young (28 +/- 2 yr) and elderly (68 +/- 3 yr) subjects underwent evaluation of renal function and blood pressure before, during, and after a 3-hour infusion of dopamine (1 microgram/kg/min) in the Clinical Research Center of Beth Israel Hospital. Renal plasma flow, estimated by clearance of para-aminohippurate clearance, was significantly lower in the elderly than in the young subjects, but both groups increased estimated renal plasma flow by approximately 30% during dopamine infusion. Endogenous creatinine clearance was also significantly lower in the elderly. During dopamine infusion, creatinine clearance rose significantly only in the young. Both young and old had a similar natriuretic response to dopamine although urine flow and free water clearance were significantly lower in the old. Neither group had significant changes in blood pressure or heart rate. Resistance to the actions of dopamine on creatinine clearance in the elderly may reflect an inability to respond to endogenous dopamine at times of physiologic stress with resulting susceptibility to azotemia.

Interleukin-2—Induced renal dysfunction in cancer patients is reversed by low-dose dopamine infusion

Recombinant interleukin-2 (rIL-2) is widely used in patients with advanced cancer to enhance killer cell functions. However, the main drawback of rIL-2 therapy is the frequent development of oliguric acute renal failure (ARF), presumably due to a vascular leak syndrome. The aim of this study was to evaluate the effect of low-dose dopamine infusion on this form of ARF. Nine patients with metastatic renal cancer and previous unilateral nephrectomy were treated with a continuous intravenous infusion of rIL-2 (3 × 10 6 Cetus units/m 2/d) for 5 days (study A). After 1 week, all the patients repeated the same cycle, but with the addition of a continuous intravenous infusion of dopamine (2 μg/min/kg body weight) that was started at the third day of treatment (study B). During study A, all patients showed a progressive (up to 34%) decrease of creatinine clearance. After rIL-2 withdrawal, these alterations persisted and were associated with a reduction in urinary output, sodium urinary excretion, and plasma protein. In study B, dopamine administration after renal function impairment (‡glomerular filtration rate = −44%) led to a prompt improvement of creatinine clearance. Creatinine clearance showed a further significant enhancement after the withdrawal of both drugs, reaching a value within the baseline range on the third day of follow-up. Similarly, the decline in urinary output and sodium excretion during rIL-2 was promptly counteracted by dopamine; in addition, after withdrawal of rIL-2 and dopamine, plasma protein levels were normalized. In conclusion, our data suggest that rIL-2-induced ARF in cancer patients is due to renal hypoperfusion mainly caused by a reduction in oncotic pressure. Importantly, intravenous infusion of dopamine at low dosage is effective in reversing this form of renal impairment; such a therapeutic approach, while reducing recovery time, avoids dose reduction or discontinuation of rIL-2 treatment.

Modification of the diuretic and natriuretic effects of a dopamine infusion by fluid loading in preoperative cardiac surgical patients

An intravenous infusion of dopamine at 2.5 microgram/kg/min was administered for 40 minutes to anesthetized cardiac surgical patients, and their renal function was measured. Five patients had the usual preoperative regimen of reduced fluid intake for the night and morning before surgery (nonhydrated), and five patients received normal saline, 2 mL/kg/hr intravenously, for 6 hours before anesthesia (hydrated). Renal function (measured by urine output, sodium excretion, free water clearance, and fractional excretion of sodium) was similar immediately before starting the dopamine infusion. All four variables were significantly higher in the hydrated group after 10 minutes; this difference becoming maximal after 40 minutes. Twenty minutes after stopping the dopamine infusion, renal function was similar in the two groups. This study indicates that preoperatively fluid-restricted patients demonstrate powerful salt and water conservation with reduced natriuretic and diuretic responses to a low-dose dopamine infusion when compared with hydrated patients. Patients with adequate fluid loading and intravascular volume will demonstrate a marked natriuresis and diuresis in response to low-dose dopamine infusion.

Quantitative Effects of Low-Dose Dopamine on Urine Output in Oliguric Surgical Intensive Care Unit Patients

Objective:To quantify the magnitude and time course of the effect of low-dose dopamine (2.5 μg/kg/min) infusions on urine output in oliguric patients.Design:A prospective, clinical study.Setting:A surgical intensive care unit (ICU) at a university hospital.Patients:A total of 19 surgical ICU patient

Effect of Metoclopramide on Renal Vascular Resistance Index and Renal Function in Patients Receiving a Low-Dose Infusion of Dopamine

Metocloprarnide is a dopamine receptor antagonist and, in large doses, has been shown to reverse the increase in renal blood flow, the diuresis and the natriuresis produced by a low-dose infusion of dopamine. We gave a single i. v. dose of metocloprarnide 10 mg to 21 patients on an intensive care unit who were haemodynamically stable and receiving dopamine 3 μg kg−1 min−1 Renal vascular resistance index, measured by duplex Doppler ultrasonography, did not change after metoclopramide. Renal function, measured by creatinine and osmolar clearance, natriuresis, kaliuresis and excretion fractions of sodium and potassium did not change after metoclopramide. We conclude that normal doses of metoclopramide (

Quantitative effects of low-dose dopamine on urine output in oliguric surgical intensive care unit patients.

To quantify the magnitude and time course of the effect of low-dose dopamine (2.5 micrograms/kg/min) infusions on urine output in oliguric patients. A prospective, clinical study. A surgical intensive care unit (ICU) at a university hospital. A total of 19 surgical ICU patients with oliguria (< 0.5 mL/kg/hr) after resuscitation to pulmonary artery occlusion pressures > 10 mm Hg, mean arterial pressures > 65 mm Hg, and cardiac index > 2 L/min/m2. Patients with acute renal failure and those patients receiving diuretics were excluded. Urine output was monitored hourly before and after dopamine was instituted for the treatment of oliguria. Spot urine electrolyte determinations and urine specific gravity measurements were obtained. Patients with urine output improvement (> 50% increase) had dopamine stopped after 4 hrs. If urine output decreased to < 0.5 mL/kg/hr, dopamine was resumed. There were no dopamine-induced changes in heart rate, pulmonary artery occlusion pressure, mean arterial pressure, or cardiac index. Mean urine output increased from 0.29 to 1.04 mL/kg/hr (p < .001) while patients were receiving dopamine. Time-to-peak response to dopamine was 7 hrs. Urine output increased to > 0.5 mL/kg/hr in 95% of patients, doubled in 89% of patients, and exceeded 1.0 mL/kg/hr in 84% of patients. After dopamine was stopped, urine output decreased to < 0.5 mL/kg/hr in 79% of patients and responded to resumption of dopamine in 100% of patients. There were no significant changes in urine sodium concentration or specific gravity. Low-dose dopamine infusion alone produces a drug-dependent increase in urine output in oliguric, euvolemic ICU patients. Maximal effect is temporally variable.

Effects of Low-Dose Dopamine Infusion on Cardiovascular and Renal Functions, Cerebral Blood Flow, and Plasma Catecholamine Levels in Sick Preterm Neonates

Effects of 2 and 4 micrograms/kg/min dopamine infusion on cardiovascular and renal functions, cerebral blood flow (CBF) and plasma catecholamine levels were studied in sick preterm neonates during the first four days of life. Preterm infants were found to have an enhanced responsiveness to the pressor effects of dopamine during this period. Comparison of the renal effects of 2 and 4 micrograms/kg/min dopamine in 61 preterm infants indicate that 2 micrograms/kg/min dopamine induces maximum diuresis and natriuresis during the first day of life provided that systemic blood pressure is within the predicted normal range. Although administration of 4 micrograms/kg/min dopamine induces further increases in blood pressure and glomerular filtration rate, urine output and sodium excretion remain similar to that on 2 micrograms/kg/min of the drug. These findings demonstrate that the direct tubular effects of dopamine play an important role in the diuretic and natriuretic action of the drug in the one-day old preterm infant. In five preterm neonates, changes in CBF transiently paralleled the dopamine-induced alterations in systemic blood pressure indicating that autoregulation of CBF is impaired but not completely ineffective in the one-day old preterm infant. In eight term neonates, increases in blood pressure had no effect on CBF. Measurements of plasma dopamine and norepinephrine levels in 14 preterm neonates and five children suggest that decreased metabolism of dopamine may contribute to the enhanced pressor responsiveness to dopamine in sick preterm infants.(ABSTRACT TRUNCATED AT 250 WORDS)

Medical advances in the treatment of congestive heart failure.

The increased incidence and prevalence of congestive heart failure place a high priority on novel treatment strategies. Left ventricular ejection fraction remains the single most valuable measurement providing both diagnostic and prognostic insights. The most systematic approach to heart failure involves an objective assessment of functional disability, to include exercise tests such as a 6-minute walk under standardized conditions. Left ventricular dysfunction incites a host of neurohumoral compensations that are of fundamental importance in the heart failure syndrome expression. Both vasoconstrictor and vasodilator neurohormones are stimulated and provide new therapeutic opportunities. The therapeutic approach to heart failure begins with a strong emphasis on prevention, patient education, and self-participation in therapy with respect to both its monitoring and adjustment. Diuretics remain a mainstay of therapy but, in the face of severe heart failure, may become ineffectual, requiring constant infusion of loop-active diuretics, combination diuretics, or diuretics in association with concomitant low-dose dopamine infusion. Vasodilator therapy has been an important advance: combination hydralazine and nitrate therapy was initially shown to be efficacious in improving survival, and more recently, angiotensin-converting enzyme (ACE) inhibitors, in the form of enalapril, have shown incremental benefit on survival over this combination. Interestingly, there is now evidence from both SOLVD and SAVE to demonstrate an unexpected and, as yet, unexplained reduction in the frequency of both unstable angina and myocardial infarction. Although, on balance, the weight of evidence concerning the long-term efficacy of inotropic agents has been disappointing, especially as it relates to their unfavorable effects on survival, recent information on vesnarinone, an agent with a complex and diversified mechanism of action, suggests that with appropriate doses, improved symptoms and survival are possible. A substantial amount of new information from randomized placebo-controlled trials attests to the symptomatic relief, hemodynamic improvement, and gain in exercise performance achieved by digoxin. A long-term survival study is ongoing to assess its effects on mortality. beta-Blockers, especially metoprolol, appear beneficial in some patients with heart failure, possibly related to their reduction in sympathetic nervous activity and restoration of beta-receptor population, with resultant improved contractile performance, enhanced myocardial relaxation, and overall increase in cardiac efficiency. Based on available evidence, the best contemporary approach to treatment involves the use of ACE inhibitors coupled with diuretic therapy, either continuous or intermittent, to relieve central or peripheral congestion. The addition of digoxin or a hydralazine nitrate combination is a logical next step, with commencement of low-dose beta-blocker a reasonable option.(ABSTRACT TRUNCATED AT 400 WORDS)

EFFECT OF METOCLOPRAMIDE ON RENAL VASCULAR RESISTANCE INDEX AND RENAL FUNCTION IN PATIENTS RECEIVING A LOW-DOSE INFUSION OF DOPAMINE

Metoclopramide is a dopamine receptor antagonist and, in large doses, has been shown to reverse the increase in renal blood flow, the diuresis and the natriuresis produced by a low-dose infusion of dopamine. We gave a single i.v. dose of metoclopramide 10 mg to 21 patients on an intensive care unit who were haemodynamically stable and receiving dopamine 3 micrograms kg-1 min-1. Renal vascular resistance index, measured by duplex Doppler ultrasonography, did not change after metoclopramide. Renal function, measured by creatinine and osmolar clearance, natriuresis, kaliuresis and excretion fractions of sodium and potassium did not change after metoclopramide. We conclude that normal doses of metoclopramide (< 0.2 mg kg-1) do not antagonize the renal effects of a low-dose infusion of dopamine in critically ill patients.

Low-dose dopamine induces early recovery of recombinant interleukin-2—Impaired renal function

Recombinant interleukin-2 (rIL-2) can produce impairment of renal function with hypotension, fluid retention, elevated blood urea nitrogen, oliguria and low fractional sodium excretion; these side-effects are a common cause of reduction or interruption of rIL-2 infusion. The aim of this study was to investigate the control and treatment of renal toxicity induced by rIL-2 therapy. Here we show that dopamine, at a low dose of 2 micrograms/kg/min, completely prevented renal toxicity induced by rIL-2. While continuing rIL-2 therapy, 24-h continuous infusion of low-dose dopamine produced a rapid normalisation of urine output and a significant decrease in serum creatinine levels and body weight (P < 0.01), with an early and complete recovery of the rIL-2--impaired renal function: mean recovery time of renal function in patients treated with dopamine was significantly lower (P < 0.05) than in nontreated patients (4.8 days vs. 10 days, respectively).

Gastric pressure response to low dose dopamine infusion in normal man

The gastric pressure response to distension was measured during intravenous infusion of dopamine at a rate of 2 μg min −1kg −1 over 2h 50min in 5 normal volunteers to determine whether dopamine at this dose potentiated gastric adaptive relaxation, leading to a fall in gastric pressure and thus a potential delay in gastric emptying. This would be of obvious importance in patients being given dopamine at this dose to support renal function and at the same time being fed by nasogastric tube. The pressure response decreased during the first hour in all five subjects (p < 0.01). In 2 it recovered during the third hour to pre-infusion values, but in 2 it remained diminished; in 1 subject the results were equivocal. Circulating dopamine, noradrenaline and adrenaline concentrations all increased during dopamine (p < 0.05), but compared with control there was no difference in plasma free fatty acids, glycerol, cortisol or glucose concentrations. Dopamine at 2 μg min −1 kg −1 produced a transient fall in gastric pressure in all subjects, and a persistent fall in some. The changes in gastric pressures were seen at infusion rates that produced no metabolic or inotropic effects.

A comparison of dopexamine and dopamine to prevent renal impairment in patients undergoing orthotopic liver transplantation

The efficacy of low-dose dopamine as a renal protective agent was compared with that of dopexamine in patients who underwent orthotopic liver transplantation. Twelve patients who received a continuous infusion of dopexamine (1-3 micrograms/kg/minute) were matched for age, diagnosis, pre-operative creatinine clearance and blood loss with 12 patients who received a low-dose infusion of dopamine (2 micrograms/kg/minute). The catecholamine infusion was started after induction of anaesthesia and continued for 48 hours after surgery. Patients in the dopexamine group had less evidence of renal impairment and failure than those in the dopamine group during 7 days after the operation, although the differences between groups did not achieve statistical significance. Similarly there were no significant differences between the two groups in peri-operative urine output, urine/plasma osmolality ratio or creatine clearance. Dopexamine is at least as effective as dopamine for renal protection in patients who undergo liver transplantation.

The Effect of Low-Dose Dopamine Infusion on Cardiopulmonary and Renal Status in Premature Newborns With Respiratory DistLow-Dosedrome

To study the effects of infusion of low doses of dopamine hydrochloride on cardiopulmonary and renal status in premature newborns with respiratory distress syndrome, 49 newborns were randomly assigned to three groups: group 1 (18 patients) received no dopamine and was the control group; group 2 (16 patients) was infused with a dose of dopamine measuring 1.0 micrograms/kg of body weight per minute for 72 hours; and group 3 (15 patients) was infused with a dose of dopamine measuring 2.5 micrograms/kg of body weight per minute for 72 hours. Birth weights, gestational ages, post-natal ages, and cardiopulmonary status of all groups at the start of the study were comparable. Continuous infusion of these low doses of dopamine for 3 days after birth did not significantly improve levels of blood gases, acid-base balance, or clinical outcome. In newborns with systemic hypotension, dopamine improved cardiovascular status and caused early return of blood pressure to the normal range. Infusion of low doses of dopamine produced mild to moderate natriuresis and insignificant increases in glomerular filtration rate and urine volume.

Metabolic Effects of Low-Dose Dopamine Infusion in Normal Volunteers

1. Dopamine in 5% (w/v) D-glucose was infused into five healthy male volunteers at doses of 2, 5 and 10 micrograms min-1 kg-1 over three sequential periods of 45 min each. 2. Oxygen consumption, respiratory exchange ratio, blood glucose concentration and plasma levels of free fatty acids, glycerol, lactate, dopamine, adrenaline and noradrenaline were measured. The results were compared with values obtained during infusion over the same time period of the corresponding volumes of 5% (w/v) D-glucose alone. 3. Energy expenditure calculated from the oxygen consumption and the respiratory exchange ratio was higher than control values during infusion of dopamine (P less than 0.001, analysis of variance) specifically at a rate of 10 micrograms min-1 kg-1 (P less than 0.05) when it was 14% higher, but not at a rate 2 of or 5 micrograms min-1 kg-1. The plasma noradrenaline concentration was 74 and 230% and the blood glucose concentration was 21 and 36% higher than control values at 5 and 10 micrograms of dopamine min-1 kg-1, respectively (P less than 0.01). At 10 micrograms of dopamine min-1 kg-1 the plasma free fatty acid concentration was 70% and the plasma glycerol concentration was 80% higher than during the control infusion (P less than 0.01). The respiratory exchange ratio and the plasma lactate concentration were the same in the two groups and did not alter during the dopamine infusion. The plasma adrenaline concentration rose significantly (P less than 0.01), but only transiently, during dopamine infusion at a rate of 2 micrograms min-1 kg-1. 4. Dopamine at low doses has metabolic effects. It increases the blood glucose concentration and the circulating noradrenaline level at an infusion rate of 5 micrograms min-1 kg-1. It increases energy expenditure and circulating free fatty acid and glycerol levels at an infusion rate of 10 micrograms min-1 kg-1, presumably due to stimulation of lipolysis.

Renal reserve filtration capacity before and after kidney donation

Renal reserve filtration capacity (RRFC) was investigated in 20 kidney donors before and within 3 months after uninephrectomy. Glomerular filtration rate (GFR) was measured by the clearance of 125I-iothalamate, and effective renal plasma flow (ERPF) was determined by the clearance of 131I-hippurate. RRFC was tested by infusion of a low dose of dopamine, by intravenous administration of an amino acid solution and, finally, by combined infusion of amino acids and low-dose dopamine. After kidney donation, the median value of the GFR was 65% of its initial value. The median value of the ERPF was 69% of its value before uninephrectomy. The filtration fraction declined significantly from 0.251 to 0.238 (medians; P less than 0.02). Median values for dopamine-induced increases in GFR were 13.8% before and 5.3% after kidney donation (P less than 0.005). Infusion of amino acids led to an increase in GFR of 11.2% before and 9.6% after donation (NS). During combined infusion, the median values for the increases in GFR were 20.0% before and 12.6% after uninephrectomy (P less than 0.02). Median changes in ERPF before and after kidney donation were 33.4 vs. 23.0% during dopamine infusion (P less than 0.005), 10.0 vs. 8.3% during amino acid infusion (NS), and 36.2 vs. 24.3% during the combined infusion of dopamine and amino acids (P less than 0.02). Infusion of dopamine induces a decrease in renal vascular resistance, resulting in a rise in glomerular blood flow. Since RRFC tested by means of dopamine infusion was significantly decreased after kidney donation, it is concluded that glomerular hyperfiltration after kidney donation is at least partially due to a rise in glomerular blood flow.

Further studies on the mechanism of the natriuretic response to low‐dose dopamine in man: effect on lithium clearance and nephrogenic cAMP formation

The effect of intravenous infusion of low-dose dopamine on electrolyte excretion, lithium clearance, nephrogenous cAMP formation and renal haemodynamics was investigated in healthy volunteers. Dopamine significantly increased the urine flow rate by 70.6% and urinary sodium excretion by 72%, but did not change creatinine clearance, PRA or plasma levels of AVP, ANP and cAMP. Renal plasma flow significantly increased by 48.6%; the glomerular filtration rate was not changed. Lithium per se increased basal PRA, but had no effect on the increments of urine flow rate, sodium excretion and renal blood flow induced by dopamine. Dopamine significantly increased the fractional excretion of lithium (representing fractional excretion of sodium at the proximal level). The increase in urinary sodium excretion during dopamine infusion, significantly correlated with the increase in fractional excretion of lithium (r = 0.94; P less than 0.01) and the increase in nephrogenous cAMP formation (r = 0.96; P less than 0.01). No correlation was found between the increase in urinary sodium excretion and the increase in renal blood flow. In conclusion, this study confirms that low-dose dopamine increases renal blood flow and urinary sodium excretion in healthy volunteers. This natriuretic response appears to be due to interaction with proximal tubular dopamine receptors, which are positively coupled to adenylate cyclase.

Renal tubular reabsorption of sodium and water during infusion of low-dose dopamine in normal man

1. Using the renal clearance of lithium (CLi) as an index of proximal tubular outflow of sodium and water, together with simultaneous measurements of effective renal plasma flow, glomerular filtration rate (GFR) and sodium clearance (CNa), renal function and the tubular segmental reabsorption rates of sodium and water during dopamine infusion (3 micrograms min-1 kg-1) were estimated in 12 normal volunteers. 2. CNa increased by 128% (P less than 0.001). Effective renal plasma flow and GFR increased by 43% (P less than 0.001) and 9% (P less than 0.01), respectively. CLi increased in all subjects by, on average, 44% (P less than 0.001). Fractional proximal reabsorption [1-(CLi/GFR)] decreased by 13% after dopamine infusion (P less than 0.001), and estimated absolute proximal reabsorption rate (GFR-CLi) decreased by 8% (P less than 0.01). Absolute distal sodium reabsorption rate [(CLi-CNa) x PNa, where PNa is plasma sodium concentration] increased (P less than 0.001), and fractional distal sodium reabsorption [(CLi-CNa)/CLi] decreased (P less than 0.001). 3. It is concluded that natriuresis during low-dose dopamine infusion is caused by an increased outflow of sodium from the proximal tubules that is not fully compensated for in the distal tubules.