Urinary Dopamine Excretion in Conscious Rats: Effect of Carbidopa in Different States of Sodium Balance

Mühlbauer, Bernd; Oßwald, Hartmut

doi:10.1159/000173757

Cited by 5 publications

(1 citation statement)

References 13 publications

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“…These results are not surprising since conflicting results have been reported concerning dopamine values in essential AHT: similar (10, 11) as well as increased (12,13) or decreased levels (14,15) have been observed. Our data are in agreement with the fact that the involvement of ERD in resting eunatremic conditions seems to be unlikely (16,18) asking the question of the reality of a dopaminergic basal tone (17).…”

Section: Discussionsupporting

confidence: 91%

Involvement of Renal Dopaminergic System in Experimental Neurogenic Arterial Hypertension

Sanchez

Damase‐Michel²,

Tran

et al. 1995

Hypertens Res

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The effect of chronic salt loading (10 g of NaCI for a period of 7 days) on urinary dopamine release has been investigated in 3 groups of beagle dogs: normotensive dogs (group 1: n = 7), and 2 groups of dogs made hypertensive by chronic sinoaortic denervation [group 2: (n = 6) during the first 4 months after sinoaortic denervation i.e. a model of arterial hypertension with high levels of plasma catecholamines and group 3: (n = 6) one year after denervation i. e. a model of arterial hypertension with normal sympathetic tone]. In normal dogs (group 1), salt loading induced an increase in urinary dopamine excretion during the two first days after salt loading. The rise in urinary dopamine was blunted in group 2. It was not observed in group 3. Salt loading failed to change arterial pressure and heart rate in the three groups of animals. These data show an alteration of the renal dopaminergic system in hypertensive sinoaortic denervated dogs suggesting that a dopaminergic impairment can appear during the development of arterial neurogenic hypertension.(Hypertens Res 1995; 18 Suppl. I: 5187-5190)Key Words: dopamine, hypertension, sinoaortic denervation, kidneyAlthough its physiological relevance is still unclear, it is now admitted that endogenous renal dopamine (ERD) plays a role in the regulation of sodium excretion (1) through activation of specific receptors (2). Moreover, as alteration of sodium handling is one of the factors involved in pathophysiology of arterial hypertension (AHT), a great interest focuses on the potential role of ERD in this pathology. Indeed, several studies showed impairment of renal dopamine mobilization during salt loading in hypertensive models (3). Most of the time, these studies concerned models of genetic AHT. The aim of our work was to investigate whether ERD could be altered during the development of acquired AHT elicited by sinoaortic denervation in dogs. Material and MethodsNineteen beagle dogs weighting from 13 to 16 kg were studies: seven normal normotensive dogs (group 1) were compared to 12 animals made hypertensive by sinoaortic denervation (SAD) as previously described (4). Briefly, carotid and aortic nerves were cut under chloralose anesthesia (80 mg/kg iv.) during 2 successive procedures, 1 at time 0, and the second 7 weeks later. During surgery, care was taken to keep both vagal and sympathic fibers in the vagus intact. The effectiveness of baroreceptor denervation was checked by the failure of norepinephrine (2 mg/kg) to induce bradycardia and nitroglycerine (1, 3, 10 and 30 mg/kg) to induce tachycardia. During the 4 first months, AHT elicited by SAD is associated with a high level in plasma catecholamines. One year after SAD, plasma catecholamine levels return to basal values (4). Furthermore, functional (5) and histological (6) renal alterations are similar to those observed in human AHT.

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Section: Discussionsupporting

confidence: 91%

Involvement of Renal Dopaminergic System in Experimental Neurogenic Arterial Hypertension

Sanchez

Damase‐Michel²,

Tran

et al. 1995

Hypertens Res

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Renal response to amino acid infusion in rats: effect of dopamine receptor antagonists and benserazide

Mühlbauer

Hartenburg

Oßwald

1994

Naunyn-Schmiedeberg's Arch Pharmacol

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Previously, we have found that feeding is a dominant factor controlling urinary dopamine excretion (UDA) in conscious rats (Mühlbauer and Osswald 1992). Since the renal response to feeding is also characterized by an increase in glomerular filtration rate (GFR), we wanted to investigate in a first step whether the feeding-induced elevations of GFR and UDA could be causally related phenomena. Therefore, we studied the influence of dopamine synthesis and dopamine receptor blockade on the renal response to amino acid infusion (AA) in thiopental anesthetized rats. AA infusion (n = 7) increased GFR by 33 +/- 7% (P < 0.001) and UDA by 87 +/- 19% (P < 0.001). In the presence of benserazide (BZD, n = 5), an inhibitor of dopamine synthesis, infused i.v. at a dose of 30 micrograms/min/kg, UDA was suppressed to values below detection limit and the AA-induced GFR increase was abolished. Continuous intravenous infusion of the DA1 receptor antagonist SCH 23390 (SCH, n = 7) in a dose of 4.0 micrograms/kg/min did not prevent the AA-induced increase in GFR (33 +/- 3%, P < 0.001) and UDA (97 +/- 12%, P < 0.001). In contrast, S-sulpiride (SUL), a specific DA2 receptor antagonist, infused continuously i.v. in a dose of 5 micrograms/kg/min, completely abolished the AA-induced GFR increase, while UDA was increased 1.6-fold (P < 0.01). Like BZD, both dopamine receptor antagonists did not affect renal sodium excretion substantially. Our results suggest, that endogenous dopamine could act as a mediator in the renal response to amino acid infusion in the rat, most likely by activation of DA2 receptors.

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Renal response to infusion of dopamine precursors in anaesthetized rats

Mühlbauer¹,

Gleiter²,

Gies³

et al. 1997

Naunyn-Schmiedeberg's Arch Pharmacol

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In the present study the renal response to intravenous infusion of the catecholamine precursors L-dihydroxyphenylalanine (L-DOPA) or L-tyrosine was investigated in thiopentone sodium-anaesthetized Sprague-Dawley rats. Glomerular filtration rate (GFR) was assessed by renal clearance of inulin, urinary concentration of dopamine (U(DA)V) by HPLC and sodium excretion (U(Na)V) by flame photometry. We found that basal U(DA)V was 6.5 +/- 0.5 pmol/min per 100 g body weight (mean +/- SEM). Intravenous infusion of L-tyrosine at 0. 1-3.0 micromol/min dose dependently enhanced U(DA)V (17 +/- 3 to 144 +/- 14 pmol/min respectively) with higher doses of L-tyrosine resulting in no further increase in U(DA)V. Compared with L-tyrosine administration significantly lower doses of L-DOPA (0.07 to 35 nmol/min) caused increases in U(DA)V which were orders of magnitude higher (18 +/- 1 to 7800 +/- 470 pmol/min, respectively) and did not show saturation characteristics. GFR did not change in response to L-tyrosine or L-DOPA infusion. No variations in urinary flow rate or in U(Na)V could be observed which were significantly correlated to changes in U(DA)V. In contrast, intravenous infusion of dopamine at a dose of 6 nmol/min significantly increased GFR by 35 +/- 6.2% and urinary flow rate by over 2-fold. Immunohistochemistry with light microscopy revealed no tyrosine hydroxylase in the kidney. Therefore, dopamine synthesis in the tubular cells mainly depends on the renal supply of L-DOPA. The unchanged GFR and U(Na)V in spite of large variations of U(DA)V argue against the hypothesis that intratubular dopamine plays a functional role in the regulation of hemodynamics or sodium transport in the kidney. Renal dopamine excretion may rather represent an effective pathway for the elimination of catecholamine precursors from the plasma.

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Urinary Dopamine Excretion in Conscious Rats: Effect of Carbidopa in Different States of Sodium Balance

Cited by 5 publications

References 13 publications

Involvement of Renal Dopaminergic System in Experimental Neurogenic Arterial Hypertension

Involvement of Renal Dopaminergic System in Experimental Neurogenic Arterial Hypertension

Renal response to amino acid infusion in rats: effect of dopamine receptor antagonists and benserazide

Renal response to infusion of dopamine precursors in anaesthetized rats

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