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Effect of Metoclopramide, a Dopaminergic Inhibitor, on Renin and Aldosterone in Idiopathic Edema: Possible Therapeutic Approach with Levodopa and Carbidopa
50
Citations
19
References
1979
Year
HypertensionElectrolyte DisorderPharmacotherapyLogistic AnalysisMolecular PharmacologyDopaminergic InhibitorElectrolyte DisturbanceNormal WomenEndocrine HypertensionSodium HomeostasisAntihypertensive TherapyNeuropharmacologyEndocrinologyIdiopathic EdemaPharmacologyPotassium HomeostasisAldosterone PhysiologyPlasma AldosteroneClinical PharmacologyPossible Therapeutic ApproachMedicineNephrologyAnesthesiology
Metoclopramide, a dopaminergic inhibitor, was injected (10 mg iv) in 15 normal women and in 9 patients with clinical evidence of idiopathic edema, while on a 130 meq sodium and 50-70 meq potassium diet. The subjects kept a recumbent position during the test. PRA slightly increased at 45 min (p < 0.01) in normal women, A low sodium diet (20–40 meq/day) seemed to accelerate the PRA response, which was significant at 20 min (P < 0.05). In patients with idiopathic edema, PRA consistently increased at 20, 30, and 45 min (P < 0.05). Plasma aldosterone (PA) increased significantly at 10, 20, 30, 45, and 60 min (P < 0.005) both in normal women and in patients. The absolute change of PA from 0–10 min was significantly higher in patients with idiopathic edema (P < 0.001) and preceded the increase of PRA. In 5 normal women, urinary sodium decreased and urinary potassium increased after metoclopramide. Serum electrolytes were not modified. In 2 patients with idiopathic edema and hypokalemia, the treatment with a central dopaminergic agonist (250 mg levodopa and 100 mg carbidopa) reduced PRA and PA, restored serum potassium to normal values, and increased urinary excretion of sodium. These data suggest a dopaminergic control of renin and aldosterone and an alteration of this control in idiopathic edema.
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