Peripheral dopamine in hypertension and associated conditions

Küchel, Otto

doi:10.1038/sj.jhh.1000870

Cited by 9 publications

(4 citation statements)

References 81 publications

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“…The enhanced natriuretic effect of dopamine during saline loading is probably not mediated by 20-HETE because saline loading decreases expression of P450 [59]. Taken together, these studies suggest that the synergistic effect of sodium loading on the natriuretic effect of dopamine is due to increased renal production of dopamine [60] and its accumulation into the tubular lumen, as well as to an increased inhibitory effect on sodium transporters. These actions cannot be explained by enhanced production of second messengers.…”

Section: Mechanism Of the Natriuretic Effect Of Dopamine After A Sodimentioning

confidence: 73%

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Renal dopamine and sodium homeostasis

José

Eisner

Felder

2000

Current Science Inc

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During the past decade, it has become evident that dopamine plays an important role in the regulation of fluid and electrolyte balance and blood pressure. Dopamine exerts its actions through two families of dopamine receptors, designated D1-like and D2-like, which are identical in the brain and in peripheral tissues. The two D1-like receptors--D1 and D5 receptors--expressed in mammals are linked to stimulation of adenylyl cyclase. The three D2-like receptors--D2, D3, and D4,--are linked to inhibition of adenylyl cyclase. Dopamine affects fluid and electrolyte balance by regulation of renal excretion of electrolytes and water through actions on renal hemodynamics and tubular epithelial transport and by modulation of the secretion and/or action of vasopressin, renin, aldosterone, catecholamines, and endothelin B receptors (ETB) receptors. It also affects fluid and sodium intake by way of "appetite" centers in the brain and alterations of gastrointestinal tract transport. The production of dopamine in neural and non-neural tissues and the presence of receptors in these tissues suggest that dopamine can act in an autocrine or paracrine fashion. This renal autocrine-paracrine function, which becomes most evident during extracellular fluid volume expansion, is lost in essential hypertension and in some animal models of genetic hypertension. This deficit may be caused by abnormalities in renal dopamine production and polymorphisms or abnormal post-translational modification and regulation of dopamine receptor subtypes.

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Section: Mechanism Of the Natriuretic Effect Of Dopamine After A Sodimentioning

confidence: 73%

“…Decreased renal dopamine production has been described in human essential hypertension but not in rodent genetic hypertension [60]. In both human and rodent genetic hypertension, abnormalities of dopamine receptor subtypes have been described.…”

Section: Genetics and Dopaminergic Mechanisms In Essential Hypertensionmentioning

confidence: 99%

Renal dopamine and sodium homeostasis

José

Eisner

Felder

2000

Current Science Inc

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“…It is of interest that patients with increased urinary dopamine and especially with elevated dopa were characterized more often by normal blood pressure and episodes of paroxysmal hypertension [1,9,11,12]. Therefore it may be speculated that in this group of patients hypotensive properties of dopamine might be to some extent responsible for the blood pressure pattern.…”

Section: Discussionmentioning

confidence: 98%

“…Therefore it may be speculated that in this group of patients hypotensive properties of dopamine might be to some extent responsible for the blood pressure pattern. It should also be taken into consideration that excessive amounts of dopamine secreted from the tumour may modu-late pressor effects of noradrenaline and adrenaline [9,[11][12][13][14][15][16][17].…”

Section: Discussionmentioning

confidence: 99%

Dopamine and Dopa Urinary Excretion in Patients with Pheochromocytoma–Diagnostic Implications

et al. 2001

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Pheochromocytoma, a potentially life-threatening disease, is a rare cause of hypertension. Most pheochromocytomas secrete excessive amounts of noradrenaline and adrenaline. It has been suggested by some authors that high circulating levels of dopamine and the catecholamine precursor dihydroxyphenylalanine (dopa) are more often associated with malignant rather than benign pheochromocytomas. Therefore the aim of this study was to evaluate urinary excretion of dopamine and dopa in patients with pheochromocytoma and to determine their role as a potential marker for malignancy of the tumour. We retrospectively analysed 120 consecutive patients (mean age 41 +/- 12 years) with histopathologically confirmed pheochromocytomas. All subjects were divided as follows: group 1 included patients with both elevated and normal dopamine urinary excretion; group 2 was characterized by increased and normal dopa urinary excretion. Dopamine urinary excretion was increased in all patients with malignant pheochromocytoma, but higher levels were also observed in some patients with a benign tumour included in group 1. Urinary excretion of dopa was in the normal range in all subjects with malignant pheochromocytoma. The results indicate that in some pheochromocytoma patients excessive dopamine excretion may point to malignant tumour, but is not a discriminating marker for malignancy in the whole studied group.

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Free amino acid and dipeptide changes in the body fluids from Alzheimer’s disease subjects

et al. 2006

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Our aim was to determine changes in free amino acid (FAA) and dipeptide (DP) concentrations in probable Alzheimer's disease (pAD) subjects compared with control (CT) subjects using liquid chromatography and electrospray ionization tandem mass spectrometry (LCMS2). We recruited gender- and age-matched study participants based on neurological and neuropsychological assessments. We measured FAAs and DPs in cerebrospinal fluid (CSF), plasma and urine using LCMS2 with selected reaction monitoring (SRM). Imidazole-containing FAAs (histidine, methyl-histidine), catecholamines (L-DOPA and dopamine), citrulline, ornithine, glycine and antioxidant DPs (carnosine and anserine) accounted for the major changes between CT and pAD. Carnosine levels were significantly lower in pAD (328.4 +/- 91.31 nmol/dl) than in CT plasma (654.23 +/- 100.61 nmol/dl). In contrast, L-DOPA levels were higher in pAD (1400.84 +/- 253.68) than CT (513.10 +/- 121.61 nmol/dl) plasma. These data underscore the importance of FAA and DP metabolism in the pathogenesis of AD. Since our data show changes in antioxidants, neurotransmitters and their precursors, or FAA associated with urea metabolism in pAD compared with CT, we propose that manipulation of these metabolic pathways may be important in preventing AD progression.

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Peripheral dopamine in hypertension and associated conditions

Cited by 9 publications

References 81 publications

Renal dopamine and sodium homeostasis

Renal dopamine and sodium homeostasis

Dopamine and Dopa Urinary Excretion in Patients with Pheochromocytoma–Diagnostic Implications

Free amino acid and dipeptide changes in the body fluids from Alzheimer’s disease subjects

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