Release of sympathetic neurotransmitter evoked by electrical stimulation is increased in the chronically decentralized artery.

The present study was performed to confirm our previous proposal that the increase in neurotransmitter release is responsible for the supersensitivity of chronically decentralized artery to transmural nerve stimulation (TNS) in the rabbit. The ear artery was decentralized unilaterally by removing the preganglionic fiber proximal to the superior cervical ganglion (SCG), and the ear arteries and SCG were dissected 8 weeks after the operation. The increase in the tritium overflow induced by TNS from the chronically decentralized artery, which had been incubated with 3H-noradrenaline (NA) for 1 hr, was markedly increased at lower frequencies (0.1 and 0.2 Hz) than that from the control artery, whereas there was no difference at higher frequencies (> 0.5 Hz). No difference was observed in the neuronal uptake of 3H-NA during incubation for 1 hr between the control and decentralized arteries. There was also no change in the contents of catecholamines in both the artery and SCG after chronic decentralization, when assayed by a radioenzymatic procedure. In conclusion, the results obtained indicate that the supersensitivity to TNS after chronic decentralization is not due to the deranged catecholamine uptake and storage mechanisms in adrenergic nerve terminals and augmented transmitter biosynthesis, but due to the increased release of transmitter in response to low frequencies of TNS.