Evoked release of endogenous norepinephrine in the canine saphenous vein. Inhibition by acetylcholine.

Most of the information concerning adrenergic neurotransmission in the blood vessel wall has been obtained from isolated blood vessels previously incubated with radiolabeled norepinephrine. In the present study, we determined the tissue content of norepinephrine and dopamine in the dog's saphenous vein using a radioenzymatic assay; tissue content of dopamine was 30 times less than tissue content of norepinephrine, and no epinephrine could be detected. During superfusion of isolated canine saphenous vein preparations, superfusate samples were collected for subsequent radioenzymatic analysis of norepinephrine, epinephrine, and dopamine. The basal efflux of endogenous norepinephrine declined slightly with time. Nerve stimulation caused frequency-dependent increases in tension, paralleled by increases in efflux of endogenous norepinephrine. The changes in tension were correlated significantly with the changes in norepinephrine overflow. Acetylcholine at 5 x 10~7M had no effect on basal tension or basal norepinephrine overflow. During nerve stimulation at 2 Hz and at 5 Hz, it significantly depressed the contractile response and the evoked overflow of endogenous norepinephrine. Neither dopamine nor epinephrine was detected during these superfusion studies. The present experiments introduce the means for measuring endogenous norepinephrine overflow in the canine saphenous vein, validate earlier work on this blood vessel, and, in particular, provide direct evidence for the inhibitory effect of acetylcholine on adrenergic neurotransmission in the blood vessel wall.