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CC Chiueh, Z Zukowska-Grojec, KL Kirk and IJ Kopin
In the present study 6-fluoronorepinephrine (6F-NE) is shown to be formed from 6-fluorodopamine (6F-DA) in vivo. The beta-hydroxylated fluorocompound is taken up by and stored in the adrenergic nerve terminals and can be released during sympathetic nerve stimulation. In the heart, the turnover rate of the exogenously administered 6F-NE was about the same as that of tritium-labeled norepinephrine. In the central nervous system, 6F-DA can be taken up by the nigrostriatal neurons. After depolarization of the dopaminergic neurons by potassium, 6F-DA is released along with the endogenous dopamine. Systemic administration of 6F-NE to the pithed rats produces dose-dependent increases in blood pressure but does not increase the heart rate. The vasopressor potency of 6F-NE is about the same as that of l- norepinephrine, about 2-fold greater than that of dl-norepinephrine. Combined treatment with yohimbine and prazosin antagonizes completely the vasopressor effect of 6F-NE. The duration of the pressor response to 6F-NE was twice that of dl- or l-norepinephrine. The present study indicates that 6-fluorocatecholamines fulfill the criteria for adrenergic false transmitters and may be useful in positron emission tomographic scanning for mapping specifically the adrenergic nervous system in the brain or in the peripheral sympathetic nerves.
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