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1 Department of Pharmacology, School of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania 15261; and 2 Department of Urology, Kanazawa University School of Medicine, Kanazawa, Ishikawa 920-8641, Japan
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
D1-selective (Sch-23390),
D2-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 D2
dopaminergic excitatory mechanisms.
brain ischemia; micturition reflex; glutamate; MK-801; dopamine
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