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Previous studies have suggested that catecholamine uptake may play a role in vascular responsiveness in hypertension. The current study was undertaken to characterize amine uptake and effects of its inhibition in an isolated human artery from normotensive subjects and to provide a basis for future study in hypertensive individuals. Accumulation of tritiated norepinephrine into the artery of normotensive subjects was time-dependent and 16.9-fold more than the incubation media concentration (1 microM) of amine after 60 minutes. There was a lesser accumulation of tritiated normetanephrine (3.1-fold), and it was not increased over time. Increasing the concentration of norepinephrine to 30 microM did not significantly change the proportional accumulation. Inhibition of neuronal uptake with cocaine (10 microM) reduced the average accumulation of both concentrations of tritiated norepinephrine to 3.9-fold (p less than 0.001). Inhibition of extraneuronal uptake with corticosterone alone (10 microM) had no significant effect on average accumulation of norepinephrine, and where combined with cocaine, there was no further effect of corticosterone. Neither cocaine nor corticosterone had any effects on accumulation of normetanephrine. In spite of elimination of approximately 75% of the uptake of norepinephrine, cocaine had very little potentiating effect on mechanical responses to exogenous norepinephrine and neurally released transmitter. Thus, norepinephrine uptake in human cystic artery is characteristic of neuronal uptake, but cocaine treatment has only a very modest potentiating effect on responsiveness to endogenous norepinephrine and no significant effect on responsiveness to exogenous amine.

Uptake of norepinephrine in an isolated artery from normotensive humans.