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https://doi.org/10.1097/00005344-199108000-00004
Copy DOIPublication Date: Aug 1, 1991 | |
Citations: 1 |
Collateral arteries from canine hindlimb contain less norepinephrine (NE) than control (normal branch) arteries yet they release more NE per stimulation. This study examines basal neuronal function in developing collateral arteries to determine if the mechanism responsible for this impairment includes limitations on reuptake and/or release of NE. Uptake of NE, determined by accumulation of [14C]l-NE, was significantly less in collateral arteries compared to branch arteries. Cocaine (10(-5)M) decreased the rate of uptake of [14C]l-NE into branch arteries by 60% but had no effect on uptake into collateral arteries. Likewise, normetanephrine (10(-5)M) had no effect on uptake of [14C]l-NE into collateral arteries and only a slight effect on branch arteries. The rate of efflux of [14C]l-NE was greater from collateral arteries. Cocaine decreased the efflux of endogenous NE by 25-30% from collateral arteries while increasing the efflux of endogenous NE from branch arteries by 20-100%. Corticosterone (10(-4) M) and pargyline (10(-4) M) had little effect on endogenous NE efflux. These studies support the hypothesis that, compared with normal branch arteries, the decreased amount of neuro-transmitter in sympathetic neurons of collateral arteries is due to both decreased uptake and increased basal and stimulated efflux.
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