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- W2193021929 abstract "The contribution of glutamatergic and dopaminergic mechanisms to bladder hyperactivity after left middle cerebral artery occlusion was evaluated by determining the effects of intravenous cumulative doses of an N-methyl-d-aspartate (NMDA) glutamatergic antagonist (MK-801) and D 1 -selective (Sch-23390), D 2 -selective (sulpiride), or nonselective (haloperidol) dopaminergic antagonists on bladder activity in sham-operated (SO) and cerebral-infarcted (CI) rats. MK-801 (1 and 10 mg/kg) or sulpiride (3–30 mg/kg) significantly increased bladder capacity (BC) in CI but decreased or had no effect, respectively, on BC in SO. Sch-23390 (0.1–3 mg/kg) decreased BC in both SO and CI. In both CI and SO, low doses of haloperidol (0.1–1 mg/kg) increased BC, but a higher dose (3 mg/kg) reversed this effect. Administration of haloperidol (0.3 mg/kg) or sulpiride (10 mg/kg) in combination with MK-801 (0.01–10 mg/kg) markedly increased BC in CI but produced small decreases or increases in BC depending on the dose of MK-801 in SO. These results indicate that the bladder hyperactivity induced by cerebral infarction is mediated in part by NMDA glutamatergic and D 2 dopaminergic excitatory mechanisms." @default.
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- W2193021929 title "Glutamatergic and dopaminergic contributions to rat bladder hyperactivity after cerebral artery occlusion" @default.
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- W2193021929 doi "https://doi.org/10.1152/ajpregu.1999.276.4.r935" @default.
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