Recently, we demonstrated that the involvement of nitric oxide (NO) in the delayed initial recovery of cerebral blood flow (CBF) after transient cerebral ischemia is associated with altered dopamine (DA) metabolism. In this study, the effect of L-arginine, the precursor of nitric oxide, on ischemic dopamine release from the striatum was investigated in Mongolian gerbils subjected to bilateral carotid artery occlusion (15 min) alone or with reflow (2hr). Dopamine and its metabolites were measured in the striatal extracellular space dialysate after continuous perfusion (2gammal/min) of artificial extracellular fluid in the presence or absence of 15 mmol/liter L- or D-arginine or 1mmol/liter nitro-L- arginine. L-arginine but not D-arginine increased the striatal content of dopamine in pre- and postischemia whereas it it lowered the levels of dopamine and 3-methoxytyramine induced by ischemia. In contrast, nitro-L- arginine reduced the preischemic levels of dopamine and 3,4- dihydroxphenylacetic acid, and had no effect on the ischemic release of dopamine. These findings indicate that L-arginine stereospecifically modified the ischemic release and metabolism of dopamine. The data also suggest that the basal level of nitric oxide is not involved in dopamine release during ischemia but may participate in regulating dopamine release under physiological conditions.
