Accumulation and release of [3H]-5-hydroxytryptamine in saphenous veins and cerebral arteries of the dog.

Experiments were performed to examine whether isolated canine blood vessels have the ability to accumulate [3H]-5-hydroxytryptamine ([3H]-5-HT) and if so, whether the 3H-amine can be released from the tissues by stimuli known to evoke release of norepinephrine. Helical strips of saphenous veins and cerebral arteries obtained from dogs were incubated with [3H]-5-HT and mounted for superfusion. Both blood vessels take up [3H]-5-HT in a concentration-dependent manner; this accumulation is markedly reduced in veins and arteries denervated with 6-hydroxydopamine and in veins pretreated with cocaine. In saphenous veins and cerebral arteries labeled with [3H]-5-HT, a basal efflux of 3H, consisting mainly of [3H]-5-hydroxyindole-acetic acid, was observed. Electrical stimulation of the preparations evoked a frequency-dependent overflow of tritium due in part to an overflow of intact [3H]-5-HT. This stimulation-induced 3H-overflow was inhibited by tetrodotoxin and was nearly absent in denervated tissues and in veins pretreated with cocaine. In saphenous veins the overflow of 3H evoked by electrical stimulation was markedly augmented by phentolamine but not influenced by methiothepin. In the veins, both K+ and tyramine caused an overflow of [3H]-5-HT which was absent after denervation or after pretreatment of the preparations with cocaine. Our results show that the major part of the [3H]-5-HT which is taken up by the isolated blood vessels accumulates in the adrenergic nerves and that the indoleamine can be released from these nerves as a "false" transmitter, together with norepinephrine.