Urinary Dopamine and Renal Handling of L–DOPA in Fasted Spontaneously Hypertensive Rats

Dantonello, Tobias; Küster, Eberhard; Mühlbauer, Bernd

doi:10.1159/000025897

Cited by 4 publications

(2 citation statements)

References 32 publications

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“…There is strain dependence in the production of dopamine in mice and rats. Urine dopamine is lower in Sprague Dawley rats than in Dahl salt-sensitive or -resistant rats (230) or in WKY and SHRs (130). A strain of WKY rats increases uri-nary dopamine after 24 h of salt loading (486) and at 4 weeks but not at 12 weeks of age.…”

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

104

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

104

215

View full text Add to dashboard Cite

show abstract

“…The urinary excretion of DA is increased in experimental situations of sodium load [11], and defects in the DA system have been found in association with some forms of hypertension both in animals [10] and in humans [26]. In spite of these data, the importance of DA in sodium balance has been questioned [3].…”

Section: Introductionmentioning

confidence: 99%

The role of dopamine-metabolizing enzymes in the regulation of renal sodium excretion in the rat

Odlind

Reenilä

Männistö

et al. 2001

Pfl�gers Archiv European Journal of Physiology

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The intrarenal natriuretic hormone dopamine (DA) is metabolized by catechol-O-methyltransferase (COMT) and monoamine oxidase (MAO). We have previously shown that inhibition of COMT by entacapone results in a potent D1-like receptor-mediated natriuretic response. The present study was performed using anaesthetized rats to compare the importance of MAO and COMT in DA-mediated natriuresis by use of the MAO inhibitor phenelzine. Urinary sodium and DA excretion remained unchanged after MAO inhibition, while excretion of the main metabolite dihydroxyphenylacetic acid (DOPAC) decreased by 55%. The response was unaltered if 5-hydroxytryptamine receptors (5-HT1A) were blocked during MAO inhibition. We also investigated the specific renal activities of MAO and COMT in rat renal cortex during DA-influenced natriuresis. Specific COMT activity in the renal cortex was reduced by 13% after isotonic sodium loading (5% of body mass) whereas renal MAO-A and MAO-B activities remained unaltered. Furthermore, preliminary data obtained from spontaneously hypertensive rats, whose basal urinary DA excretion is higher than that of normotensive Wistar-Kyoto rats, show a tendency for renal COMT activity to be lower. It is concluded that MAOinhibition by phenelzine does not alter sodium excretion. Furthermore, specific renal cortical COMT activity is reduced during partly D1-like receptor-mediated natriuresis, whereas MAO activity remains unchanged. The results suggest that MAO is less important than COMT in regulating DA-mediated natriuresis in the rat kidney.

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