Renal response to infusion of dopamine precursors in anaesthetized rats

Mühlbauer, Bernd; Gleiter, Christoph H.; Gies, C.; Luippold, Gerd; Löschmann, Peter‐Andreas

doi:10.1007/pl00005125

Cited by 14 publications

(17 citation statements)

References 26 publications

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“…We have reported recently that infusion of L-DOPA in anesthetized normotensive rats can increase U DA V by orders of magnitude [26]. The present experiments extend this observation insofar as no strain-related differences in the enormous capacity of renal dopamine formation were detected comparing SHR, WKY, and SD animals.…”

Section: Discussionsupporting

confidence: 76%

“…This is not surprising since previous studies in normotensive rats and humans have failed to demonstrate a functional link between urinary DA and U Na V: under feeding-controlled conditions, salt loading did not alter U DA V [8,9]. Vice versa, no natriuresis was observed following stimulation of urinary DA release by L-DOPA administration in man and rat [9,26]. Consistent with these reports, no significant natriuretic or diuretic response to low-dose L-DOPA infusion occurred in spite of the 30-fold increase in U DA V when compared to baseline and the respective experimental series in the CON experiments.…”

Section: Discussionmentioning

confidence: 79%

“…In DOPA series, following baseline periods infusion was switched to L-DOPA in two consecutive doses (1 nmol and 3 µmol per minute and 100 g body weight). The low dose was demonstrated previously [26] to increase U DA V significantly in SD rats without affecting GFR, urinary flow rate (UV), or U Na V. The very high infusion rate of 3 µmol/min L-DOPA was chosen since in this dose range the U DA Vshows saturation characteristics indicating the proximity to the maximal rate of either synthesis or luminal transport of DA [27]. Due to its better solubility at neutral pH, L-DOPA ester was used.…”

Section: Clearance Experimentsmentioning

confidence: 99%

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

Dantonello

Küster²,

Mühlbauer³

1998

Kidney Blood Press Res

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A defective renal dopaminergic system has been suggested to contribute, via impaired sodium excretion, to the pathogenesis of hypertension. Data according renal dopamine (DA) release in hypertension, however, are inconsistent. In the present study, we compared urinary DA excretion (U_DAV), plasma free DA (P_DA), and renal tissue DA contents (T_DA) of young spontaneously hypertensive rats (SHR), Wistar–Kyoto (WKY), and Sprague–Dawley (SD) rats. Since the protein intake dominantly controls U_DAV, fasted animals were used to exclude the influence of feeding. Conscious WKY and SHR had a similar U_DAV which was lower compared to SD rats. Thiopental anesthesia increased U_DAV in SHR and WKY but not in SD rats. T_DA was higher in SHR compared to SD and WKY rats. To investigate the tubular capacity to generate DA, the response to L–DOPA infusion was assessed in two doses. 1 nmol/min/100 g body weight L–DOPA increased U_DAV approximately 30–fold in all strains but did not affect tubular sodium excretion or renal hemodynamics. In contrast, infusion of 3 μmol/min/100 g body weight L–DOPA increased U_DAV by five orders of magnitude and induced natriuresis, diuresis, and tachycardia. These effects were assigned to an increase in P_DA and no significant differences were observed among the strains. We conclude that, regarding renal DA, (1) the differences among SHR, WKY, and SD rats rather appear to be strain related than hypertension associated; (2) the renal capacity of DA generation from L–DOPA is not impaired in SHR; (3) tubular DA at physiological concentrations does not alter sodium excretion significantly in normo– or hypertensive rats, and (4) the influence of anesthesia on U_DAV should be considered in comparative studies.

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Section: Discussionsupporting

confidence: 76%

Section: Discussionmentioning

confidence: 79%

Section: Clearance Experimentsmentioning

confidence: 99%

See 1 more Smart Citation

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

Dantonello

Küster²,

Mühlbauer³

1998

Kidney Blood Press Res

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“…The natriuretic tubular action of dopamine, widely accepted by most authors (see for review Jose et al 1992) was not supported by a number of experiments. For instance, elevated tubular concentrations of dopamine, due to infusion of its precursors, did not increase sodium excretion (Mühlbauer et al 1997;Wang et al 1997). Reasons for the discrepant observations might be differences in species, in state of consciousness, and varying levels of extracellular volume (Hansell and Fasching 1991).…”

Section: Discussionmentioning

confidence: 99%

“…Male Sprague-Dawley rats (Charles River, Sulzfeld, Germany) weighing 240-280 g were anesthetized with thiopental (Byk Gulden, Konstanz, Germany). The preparation of the animals was described previously (Mühlbauer et al 1997). In brief, tracheostomy was performed and two PE-catheters were inserted into the right jugular vein for i.v.…”

Section: Methodsmentioning

confidence: 99%

Dopamine D3 receptor activation modulates renal function in anesthetized rats

Luippold

Küster

Joos

et al. 1998

Naunyn-Schmiedeberg's Arch Pharmacol

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The renal effects of the D3 receptor agonist R(+)-7-hydroxy-dipropyl-aminotetraline (7-OH-DPAT) were studied in anesthetized Sprague-Dawley rats using standard clearance experiments. 7-OH-DPAT infusion (0.01, 0.1, and 1.0 microg kg(-1) min(-1)) dose-dependently increased glomerular filtration rate (GFR) compared to baseline by a maximum of 20+/-2% while arterial blood pressure was not affected. Heart rate was not altered during the two lower doses of 7-OH-DPAT whereas a slight reduction occurred due to infusion of 1.0 microg kg(-1) min(-1). In contrast, higher doses of 7-OH-DPAT, starting from 3 microg kg(-1) min(-1), markedly influenced systemic hemodynamics. In addition to the hyperfiltration, 7-OH-DPAT (1.0 microg kg(-1) min(-1)) also induced a significant diuresis (27.7+/-4.3 microl min(-1) 100 g(-1) vs 16.2+/-5.4 microl min(-1) 100 g(-1)) and increased both absolute (3.30+/-0.58 micromol min(-1) 100 g(-1) vs 0.95+/-0.26 micromol min(-1) 100 g(-1)) and fractional sodium excretion (2.48+/-0.32% vs 0.79+/-0.19%). These changes in renal function were not modulated by pretreatment with the D2 receptor antagonist S(-)-sulpiride but abolished by the D3 antagonist 5,6-dimethoxy-2-(di-n-propylamino)indane (U-99194A). In coincidence with the action of 7-OH-DPAT on both glomerular and tubular function, reverse transcription-polymerase chain reaction (RT-PCR) revealed the expression of D3 receptors in both glomerular and tubular fractions of kidneys taken from Sprague-Dawley rats. These data indicate that D3 receptors in the kidney are involved in the regulation of renal hemodynamics and tubular function.

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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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Renal response to infusion of dopamine precursors in anaesthetized rats

Cited by 14 publications

References 26 publications

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

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

Dopamine D3 receptor activation modulates renal function in anesthetized rats

Dopamine and Renal Function and Blood Pressure Regulation

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