Blackwell Publishing Journal Backfiles 1879-2005
—A method for perfusion of rat brain ventricles accompanied by electrical stimulation of right vagus nerve was used in the study of the re-uptake mechanism of norepinephrine in rat brain. Tritiated norepinephrine was injected into the left lateral brain ventricle. After a 1-hr equilibration period, the brain was perfused, and effluent was collected and assayed for norepinephrine, normetanephrine and acid metabolites by means of column chromatography and liquid scintillation counting. Electrical stimulation of central end of right vagus nerve produced a significant release of norepinephrine and decrease of acid metabolites; this indicates a shift of catecholamines to extracellular sites. Angiotensin (200 ng/min) added to the perfusion fluid potentiated the effect of nerve stimulation. Cocaine, desmethylimipramine and phenoxybenzamine greatly reduced the release of norepinephrine from brain tissue. None on these drugs potentiated the effect of angiotensin. It is concluded that angiotensin prevents re-uptake of norepinephrine released by nerve stimulation. As a naturally occurring, physiologically active peptide, angiotensin seems to be highly specific in modulation of adrenergie neurotransmission, allowing increased extraneuronal accumulation of neurotransmitter.
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