Diagnostic Significance of Dopamine Estimation Using Plasma and Urine in Patients with Adrenal and Renal Insufficiency, Renal Transplantation and Hypertension

Yoshimura, Manabu; Komori, Toshiaki; Nishimura, Masato; Habuchi, Yoshizumi; Fujita, Naohisa; Nakanishi, Tadashi; Yasumura, Tadaki; Takahashi, Hakuo

doi:10.1291/hypres.18.supplementi_s87

Cited by 10 publications

(5 citation statements)

References 24 publications

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“…Urinary excretion of dopamine (21) and urinary dopamine response to high salt are also decreased in aged rats (632). Urinary excretion of dopamine is decreased in patients with renovascular hyper-tension, chronic renal insufficiency and failure (300,478,693) in whom the reduced activity of their renal dopaminergic system correlates well with the degree of deterioration of renal function. Patients with primary aldosteronism (333) and women with pre-eclampsia (475) have increased urinary dopamine.…”

Section: Structure and Function Of The Renal Dopaminergic Systemmentioning

confidence: 99%

Dopamine and Renal Function and Blood Pressure Regulation

Armando

Villar

José

2011

Comprehensive Physiology

108

215

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Dopamine is an important regulator of systemic blood pressure via multiple mechanisms. It affects fluid and electrolyte balance by its actions on renal hemodynamics and epithelial ion and water transport and by regulation of hormones and humoral agents. The kidney synthesizes dopamine from circulating or filtered L-DOPA independently from innervation. The major determinants of the renal tubular synthesis/release of dopamine are probably sodium intake and intracellular sodium. Dopamine exerts its actions via two families of cell surface receptors, D1-like receptors comprising D1R and D5R, and D2-like receptors comprising D2R, D3R, and D4R, and by interactions with other G protein-coupled receptors. D1-like receptors are linked to vasodilation, while the effect of D2-like receptors on the vasculature is variable and probably dependent upon the state of nerve activity. Dopamine secreted into the tubular lumen acts mainly via D1-like receptors in an autocrine/paracrine manner to regulate ion transport in the proximal and distal nephron. These effects are mediated mainly by tubular mechanisms and augmented by hemodynamic mechanisms. The natriuretic effect of D1-like receptors is caused by inhibition of ion transport in the apical and basolateral membranes. D2-like receptors participate in the inhibition of ion transport during conditions of euvolemia and moderate volume expansion. Dopamine also controls ion transport and blood pressure by regulating the production of reactive oxygen species and the inflammatory response. Essential hypertension is associated with abnormalities in dopamine production, receptor number, and/or posttranslational modification.

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Section: Structure and Function Of The Renal Dopaminergic Systemmentioning

confidence: 99%

Dopamine and Renal Function and Blood Pressure Regulation

Armando

Villar

José

2011

Comprehensive Physiology

108

215

View full text Add to dashboard Cite

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“…Chronic renal parenchymal diseases are accompanied by progressive loss of tubular functional units endowed with AADC, and preliminary evidence has suggested that the urinary excretion of free dopamine may be reduced in these disorders [15]. The aim of the present study was at examine the relationship between the renal function and the daily urinary excretion of L-DOPA, free dopamine, DOPAC and HVA in patients with chronic renal parenchymal disease, in conditions of controlled sodium, potassium and phosphate intake, and gather information on the renal dopaminergic system activity, in these conditions.…”

Section: Introductionmentioning

confidence: 99%

Reduced Urinary Excretion of Dopamine and Metabolites in Chronic Renal Parenchymal Disease

Pestana¹,

Jardim

Serrão

et al. 1998

Kidney Blood Press Res

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Background: Chronic renal parenchymal diseases are accompanied by a progressive loss of tubular units endowed with the ability to synthesise dopamine from L-3,4-dihydroxyphenylalanine (L-DOPA), and preliminary evidence has suggested that the urinary excretion of free dopamine may be reduced in these disorders. However, it is well recognised now that under in vitro conditions, dopamine newly synthesised in tubular epithelial cells undergoes extensive deamination to 3,4-dihydroxyphenylacetic acid (DOPAC) by monoamine oxidase (MAO); a small amount of the amine is converted to homovanillic acid by both MAO and catechol-O-methyltransferase (COMT) and a minor amount is methylated to 3-methoxytyramine. Aims: The present study aimed at examining the relationship between renal function and daily urinary levels of L-DOPA, free dopamine and its main metabolites, DOPAC and homovanillic acid (HVA) in patients (n = 28) with chronic renal parenchymal disease, in conditions of controlled sodium, potassium and phosphate intake. The levels of 5-hydroxyindolacetic acid (5-HIAA) were also evaluated in the same cohort of patients. Results: The patients were divided in two groups according to creatinine clearance (group 1, 39±6 ml/min/1.73 m², n = 14; group 2, 139±6 ml/min/1.73 m², n = 14). In patients of group 1, the urinary levels of L-DOPA, dopamine and DOPAC (in nmol/24 h) were significantly lower (60% reduction) than in patients of group 2 (L-DOPA, 134±36 vs. 308±51; dopamine, 759± 175 vs. 1,936± 117; DOPAC 2,595±340 vs. 7,938±833). Also, the urinary excretion of HVA in patients group 1 was significantly lower (40% reduction) than in patients of group 2 (17,434±2,455 vs. 27,179±2,271 nmol/24 h). By contrast, no significant difference was observed in daily urinary excretion of 5-HIAA between the two groups of patients (group 1, 27,280±3,721 nmol/day; group 2, 28,851±2,854 nmol/day). A positive linear relationship was found in these 28 patients between the creatinine clearance and the daily urinary excretion of L-DOPA (r = 0.64, p < 0.001), free dopamine (r = 0.83; p < 0.0001), DOPAC (r = 0.86; p < 0.0001) and HVA (r = 0.65; p < 0.002), but not with that of 5-HIAA (r = 0.14; ns). The U_{dopamine/L-DOPA} and U_{DOPAC/dopamine} ratios were found to be similar in both groups of patients, whereas the U_HVA/DOPAC ratios in patients of group 1 were found greater than in group 2 (p < 0.05). Conclusion: Patients suffering from chronic parenchymal disease with a compromised renal function present with a reduced activity of their renal dopaminergic system which correlates well with the degree of deterioration of renal function. The reduced urinary dopamine output in renal insufficiency is not attributable to enhanced metabolism of renal dopamine. We suggest that the urinary levels of DOPAC may represent a useful parameter for the assessment of renal dopamine synthesis.

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“…Nevertheless, it is believed to be clinically useful. 18 In this study, samples were collected in standardized bottles with preservative, protected from ultraviolet light, and refrigerated to help stabilize the dopamine compound, and we did see a significant reduction in dopamine excretion with carbidopa. We could not measure the concentration of dopamine in the area postrema, a known vomiting center, 7 but we did find a significant correlation between free dopamine in the urine and symptom severity (figure 1).…”

Section: Resultsmentioning

confidence: 73%

Hyperdopaminergic crises in familial dysautonomia

et al. 2013

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Objective: The purpose of this study was to determine whether carbidopa (Lodosyn), an inhibitor of dopa-decarboxylase that blocks the synthesis of dopamine outside the brain, is an effective antiemetic in patients with familial dysautonomia (FD) and hyperdopaminergic nausea/retching/vomiting attacks. Methods:We enrolled 12 patients with FD in an open-label titration and treatment study to assess the safety of carbidopa. We then conducted a randomized, double-blind, placebo-controlled, crossover study to evaluate its antiemetic efficacy.Results: Previous fundoplication surgery in each patient studied prevented vomiting, but all of the subjects experienced severe cyclical nausea and uncontrollable retching that was refractory to standard treatments. Carbidopa at an average daily dose of 480 mg (range 325-600 mg/day) was well tolerated. In the double-blind phase, patients experienced significantly less nausea and retching while on carbidopa than on placebo ( p , 0.03 and p , 0.02, respectively). Twenty-fourhour urinary dopamine excretion was significantly lower while on carbidopa (147 6 32 mg/gCr) than while on placebo (222 6 41mg/gCr, p , 0.05).Conclusions: Carbidopa is a safe and effective antiemetic in patients with FD, likely by reducing the formation of dopamine outside the brain. Recurrent bouts of nausea, retching, and vomiting accompanied by tachycardia and hypertension following emotional or physiologic stresses are a common disabling feature of familial dysautonomia (FD) (Riley-Day syndrome or hereditary sensory and autonomic neuropathy type III).1,2 Standard antiemetics have little effectiveness during these episodes. Traditionally, patients with FD were advised to manage their episodes with benzodiazepines.3 Many quickly become tolerant and require increasing doses, which have been associated with respiratory depression. The central sympatholytic agent, clonidine, has been used with some success, but its use is limited by the unwanted side effects of sedation and hypotension.3 Metoclopramide has also been used, but it is frequently associated with tardive dyskinesia, and is therefore not suitable as a long-term therapy. 4 Newer agents like pregabalin are only moderately effective. 5Because of a developmental abnormality in the afferent neurons of the baroreflex, patients with FD are unable to restrain sympathetic outflow.6 Vomiting/retching attacks occur during sympathetic activation when dopamine spills over into the circulation. 2 We hypothesize, therefore, that vomiting is due to activation of dopamine receptors in the chemoreceptor trigger zone, which lies outside the blood-brain barrier. The purpose of this study was to determine whether carbidopa (Lodosyn, Merck & Co., Inc., Whitehouse Station, NJ), an inhibitor of dopa-decarboxylase that blocks the synthesis of dopamine outside the brain, 8 is an effective antiemetic in patients with FD. We present the results of a randomized, placebo-controlled trial conducted in patients with FD.

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Diagnostic Significance of Dopamine Estimation Using Plasma and Urine in Patients with Adrenal and Renal Insufficiency, Renal Transplantation and Hypertension

Cited by 10 publications

References 24 publications

Dopamine and Renal Function and Blood Pressure Regulation

Dopamine and Renal Function and Blood Pressure Regulation

Reduced Urinary Excretion of Dopamine and Metabolites in Chronic Renal Parenchymal Disease

Hyperdopaminergic crises in familial dysautonomia

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