Metoclopramide Does Not Affect Renal Function and Atrial Natriuretic Peptide Release in Response to Acute Saline Loading in Conscious Rats

Nati, Romain; Campean, Michael; Kramer, Herbert J.

doi:10.1159/000139167

Cited by 4 publications

(3 citation statements)

References 36 publications

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“…Precise mechanisms of these two pathways are presently unclear, but saline expansion might have dissected the existence of such contradictory dual pathways. Using conscious rats injected with MCP under isotonic ECFV expansion, Nati et al (1994) reported and discussed a role of DA acting via DA2 receptors on renal Na excretion (7). However, our low dose of DA infusion experiment in saline volume-expanded dogs would be explained by a model in which multiple subtypes of DA and multiple second messengers have effects on Na-linked transporters and Na-pump for the modulation of natriuresis.…”

Section: Discussionmentioning

confidence: 99%

Dopamine Tonically Modulates Natriuresis in the Saline-Expanded Dogs

Honda

Nunokawa

Matsuzaki³

et al. 1995

Hypertens Res

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Dopamine (DA) has been shown to be an endogenous catecholamine that promotes natriuresis by activating tubular DA receptors, but its role on natriuresis appears to be equivocal, and the precise mechanisms and signaling pathway of multiple DA's receptor subtypes are not yet clarified. We used low dose of DA intravenously in saline (S) volume-expanded dogs to see the alterations in natriuresis. The results showed that there is a critical dose that induces no enhancement of natriuresis of volume expansion, and that the lower and higher doses of DA produced relatively larger natriuresis. Pretreatment of metoclopramide (MCP) in this settings caused even higher and significant increases of natriuresis. In conclusion, DA seems to determine tonically the level of natriuresis in saline-expanded dogs. DA may exert a dual effect on signal transduction pathways such that one leading to antinatriuresis with high affinity and the other to natriuresis with low affinity signaling cascades for DA. MCP may block the antinatriuretic limb of the signaling pathway.

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Section: Discussionmentioning

confidence: 99%

Dopamine Tonically Modulates Natriuresis in the Saline-Expanded Dogs

Honda

Nunokawa

Matsuzaki³

et al. 1995

Hypertens Res

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“…Different physiological factors and systems, such as physical factors, prostaglandins, dopamine and NO, have been also found. [15][16][17] In view of the proposed role of L-Arg in regulating sodium and water excretion, we considered that L-Arg may contribute to the diuretic and natriuretic response during volume expansion. Thus, the present study was undertaken to elucidate the effects of L-Arg on blood pressure and renal function during extracellular fluid volume expansion in rats and to determine whether diuretic treatment with FUR can be optimized by the co-administration of L-Arg in this model.…”

Section: Introductionmentioning

confidence: 99%

“…Although atrial natriuretic factor has been reported to contribute to this phenomenon, it is not the only substance involved in the natriuretic response. Different physiological factors and systems, such as physical factors, prostaglandins, dopamine and NO, have been also found 15–17 …”

Section: Introductionmentioning

confidence: 99%

Effects Of L‐Arginine And Furosemide On Blood Pressure And Renal Function In Volume‐Expanded Rats

Costa

Marchetti

Balaszczuk

et al. 2001

Clin Exp Pharma Physio

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1. The aim of the present study was to investigate the effects of L-arginine (L-Arg) on blood pressure and water and electrolyte excretion in control and extracellular fluid volume-expanded rats (10% bodyweight with 0.9% NaCl) and to determine whether diuretic treatment with furosemide (FUR) can be optimized by the administration of L-Arg in this model. 2. Both groups of animals were anaesthetized, divided into groups and treated with either 7.5 mg/kg FUR, 250 mg/kg L-Arg, 1 mg/kg NG-nitro-L-arginine methyl ester (L-NAME), FUR + L-NAME or FUR + L-Arg. Mean arterial pressure (MAP), diuresis, natriuresis and kaliuresis were determined. 3. Extracellular fluid volume expansion induced no changes in MAP in control and volume-expanded rats (92+/-6 vs 100+/-8 mmHg, respectively). The hypotension induced by FUR in control and volume-expanded rats (69+/-7 and 76+/-5 mmHg, respectively) was significantly (P < 0.01) enhanced by the administration of L-Arg (54+/-3 and 64+/-3 mmHg, respectively). 4. Injection of L-NAME increased MAP and diminished diuresis, natriuresis and kaliuresis in both groups. 5. Furosemide-induced water and electrolyte excretion was blunted by the administration of L-NAME. 6. The combination of L-Arg + FUR increased diuresis induced by FUR alone (control rats: 29.33+/-1.68 vs 12.91+/- 0.41 microL/min per 100 g, respectively; volume-expanded rats: 248.5+/-25.4 vs 112,6+/-8.3 microL/min per 100 g, respectively; P < 0.01). 7. The administration of the combination of L-Arg + FUR promoted a decrease in the sodium/water excretion ratio compared with the administration of FUR alone (control rats: 0.230+/-0.018 vs 0.45+/-0.03, respectively, P < 0.001; volume-expanded rats: 0.091+/-0.010 vs 0.22+/-0.03, respectively, P < 0.01). 8. The potassium/water excretion rate induced by FUR alone and in the presence of L-Arg followed a pattern similar to that seen for natriuresis (control rats: 0.35+/-0.05 vs 0.20+/-0.05 microEq/min per 100 g, respectively; volume-expanded rats: 0.045+/-0.008 vs 0.014+/-0.003 microEq/min per 100 g, respectively; P < 0.01). 9. The decrease in the electrolyte/water excretion ratio observed with FUR + L-Arg in volume-expanded rats was greater than in control animals. 10. The results of the present study show that the administration of FUR with L-Arg contributes to enhanced hypotensive and diuretic effects of FUR, thus diminishing the relative electrolyte excretion in normal conditions and in extracellular fluid volume expansion.

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