Impaired Renal Hemodynamic but Conserved Natriuretic Response to Dopamine in Patients with Renal Disease

Smit, Andries J.; Meijer, S; Wesseling, H; Reitsma, Wd; Donker, A. J. M.

doi:10.1159/000185674

Cited by 23 publications

(21 citation statements)

References 8 publications

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“…This increased loss is not sustained with chronic use of glucocorticoids and has not been seen by all investigators. Dopamine in doses of 0.25-8 mg.kg À1 .min À1 has been shown to have a phosphaturic effect both in healthy volunteers and in patients with renal failure [36].…”

Section: Loss Of Phosphate From the Bodymentioning

confidence: 99%

HypophosphataemiaPathophysiology, effects and management on the intensive care unit

1998

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SummaryRoutine detection and treatment of hypophosphataemia on the intensive care unit is commonplace. Hypophosphataemia has been associated with a multitude of clinical effects and there are many associations between correction of hypophosphataemia and improvement in symptoms. However, there is no evidence at present to support the routine correction of hypophosphataemia in the absence of clinical symptoms or signs.

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Section: Loss Of Phosphate From the Bodymentioning

confidence: 99%

HypophosphataemiaPathophysiology, effects and management on the intensive care unit

1998

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“…In a recent study, doseresponse analysis of dopamine in water-loaded individuals was performed. 103 It was found that the natriuretic and renal vasodilating effect of dopamine was maximal at a dose of 3 g ⅐ kg Ϫ1 ⅐ min…”

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confidence: 99%

Renal Dopamine Receptor Function in Hypertension

1998

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Abstract-Dopamine plays an important role in the regulation of renal sodium excretion. The synthesis of dopamine and the presence of dopamine receptor subtypes (D 1A , D 1B as D 1 -like and D 2 , and D 3 as D 2 -like) have been shown within the kidney. The activation of D 1 -like receptors located on the proximal tubules causes inhibition of tubular sodium reabsorption by inhibiting Na,H-exchanger and Na,K-ATPase activity. The D 1 -like receptors are linked to the multiple cellular signaling systems (namely, adenylyl cyclase, phospholipase C, and phospholipase A 2 ) in the different regions of the nephron. Defective renal dopamine production and/or dopamine receptor function have been reported in human primary hypertension as well as in genetic models of animal hypertension. There may be a primary defect in D 1 -like receptors and an altered signaling system in the proximal tubules that lead to reduced dopamine-mediated effects on renal sodium excretion in hypertension. Recently, it has been shown in animal models that the disruption of either D 1A or D 3 receptors at the gene level causes hypertension in mice. Dopamine and dopamine receptor agonists also provide therapeutic potential in treatment of various cardiovascular pathological conditions, including hypertension. However, because of the poor bioavailability of the currently available compounds, the use of D 1 -like agonists is limited to the management of patients with severe hypertension when a rapid reduction of blood pressure is clinically indicated and in acute management of patients with heart failure. In conclusion, there is convincing evidence that dopamine and dopamine receptors play an important role in regulation of renal function, suggesting that a defective dopamine receptor/signaling system may contribute to the development and maintenance of hypertension. Further studies need to be directed toward establishing a direct correlation between defective dopamine receptor gene in the kidney and development of hypertension. Subsequently, it may be possible to use a therapeutic approach to correct the defect in dopamine receptor gene causing the hypertension. (Hypertension. 1998;32:187-197.)Key Words: dopamine Ⅲ receptors, dopamine Ⅲ kidney tubules, proximal Ⅲ kidney Ⅲ hypertension, renal D opamine is known to play an important role in the control of renal sodium excretion. Specific receptors for dopamine have been identified in various regions of the nephron, and it is reported that dopamine is synthesized within the renal proximal tubules. Endogenously produced dopamine, as well as exogenously administered dopamine, exerts pronounced effects on renal function. There are reports suggesting that a defect in renal dopamine receptor function and/or dopamine production may play a role in the pathogenesis of hypertension. For example, reduced urinary dopamine/ sodium excretion is reported in some forms of human primary hypertension. [1][2][3] It is reported that a defect in dopamine receptor-G protein coupling and alterations in the signaling component...

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“…Corroborating our results, other authors have also shown that renal function is not improved with LDD for patients undergoing cardiac surgery 16 or liver transplantation, 17 or for those in postoperative states, 15,16,31 critically ill with oliguria, 13 or with previous renal diseases. 14 Other recent studies have confirmed these findings. In a double-blind, randomized, multicenter, placebo-controlled study with a large number of severely ill patients (n = 328), 18 treatment with LDD did not seem to be advantageous.…”

Section: Discussionmentioning

confidence: 52%

“…The effect of LDD on natriuresis may be explained by its inhibition of aldosterone, 14 and by its direct action on the proximal renal tubules. 10 In some studies in which a significant increase in sodium excretion was detected, the patients were suffering from congestive cardiac failure, 4,12 but other studies have found higher excretion even in patients without cardiac disease.…”

Section: Referencesmentioning

confidence: 99%

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Hemodynamics and renal function during administration of low-dose dopamine in severely ill patients

et al. 2004

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CONTEXT: Although a large number of studies have been performed regarding the renal and hemodynamic effects of the infusion of low-dose dopamine (LDD) in severely ill patients, there is still controversy on this subject. OBJECTIVE: To evaluate the effects of dopamine (2 mug/kg/min) on systemic hemodynamics (lowest mean arterial pressure, MAP, highest heart rate, HR, central venous pressure, CVP), creatinine clearance (CLcr), diuresis and fractional sodium excretion (FENa+). TYPE OF STUDY: A non-randomized, open, prospective clinical trial. SETTING: An intensive care unit in a tertiary university hospital. PARTICIPANTS: 22 patients with hemodynamic stability admitted to the intensive care unit. PROCEDURES: Patients were submitted to three two-hour periods: without dopamine (P1), with dopamine (P2) and without dopamine (P3). MAIN MEASUREMENTS: The abovementioned variables were measured during each period. CLcr was assessed based upon the formula U x V/P, where U is urinary creatinine (mg/dl), V is diuresis in ml/min and P is serum creatinine (mg/dl). FENa+ was calculated based upon the formula: urinary sodium (mEq/l) x P/plasma sodium (mEq/l) x U) x 100. Results were presented as mean and standard deviation. The Student t test was used and results were considered significant if p was less than 0.05. RESULTS: Twelve patients (seven males and five females) were included, with a mean age of 55.45 years. There was no significant variation in MAP, HR, CVP, CLcr or FENa+ with a dopamine dose of 2 mug/kg/min. On the other hand, diuresis significantly increased during P2, from 225.4 to 333.9 ml. CONCLUSION: Infusion of 2 mug/kg/min of dopamine for 2 hours increases diuresis. At the doses studied, dopamine does not induce significant alterations in MAP, HR, CVP, CLcr and FENa+.

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Impaired Renal Hemodynamic but Conserved Natriuretic Response to Dopamine in Patients with Renal Disease

Cited by 23 publications

References 8 publications

HypophosphataemiaPathophysiology, effects and management on the intensive care unit

HypophosphataemiaPathophysiology, effects and management on the intensive care unit

Renal Dopamine Receptor Function in Hypertension

Hemodynamics and renal function during administration of low-dose dopamine in severely ill patients

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