On the Role of Neuronal Uptake (Uptake1) in the Inactivation of Noradrenaline by Aortic Strips

Abstract

Inactivation of exogenous and neural noradrenaline was investigated in isolated rabbit aortic strips by a combination of the techniques of transmural stimulation and oil immersion. The latter technique was found to be a simple and reliable method for estimation of inhibition of the various intrinsic tissue pathways for inactivation of noradrenaline. Half-relaxation times ([Formula: see text]'s) of exogenous-noradrenaline responses were significantly increased by tropolone and cocaine. Cocaine had a slightly greater effect, increasing [Formula: see text] to 1.7–2.0 times the control value; tropolone increased [Formula: see text] to 1.2–1.3 times the control value. Iproniazid, tropolone and cocaine all significantly increased the [Formula: see text]'s of neural-noradrenaline responses. The enzyme inhibitors caused increases of 1.3–1.9, and cocaine, increases of 9–15 times the [Formula: see text]'s of neural-noradrenaline responses. Cocaine had a variable small effect on [Formula: see text]'s of responses to exogenous noradrenaline in aortic strips denervated by cold storage, and it is inferred that the post-junctional effect of cocaine contributes little to its effect on [Formula: see text]'s of fresh tissue. In conclusion, it is estimated that neuronal uptake can account for the disposition of approximately 50% of exogenous noradrenaline and 90% of neural noradrenaline in rabbit aortic strips. Studies with the oil-immersion technique and exogenous noradrenaline have probably underemphasized the importance of neuronal uptake in vascular tissue.