Infusions of adrenaline stimulate noradrenergic transmission in man, but adrenaline is not released later as a co-transmitter.

A pre-junctional beta-adrenoceptor facilitating noradrenergic transmission may be affected by elevations in circulating adrenaline, and represent a mechanism whereby mental stress might predispose to hypertension. The proposition that circulating adrenaline can be taken up into noradrenergic nerve terminals and later co-released with noradrenaline in response to an appropriate stimulus was examined. The effects of upright posture, before and after a 60 min adrenaline infusion were as follows: (1) Changes in heart rate and diastolic blood pressure were not augmented. (2) Plasma noradrenaline response was not increased. (3) Plasma adrenaline basally and in response to posture remained low. (4) Radiolabelled adrenaline disappeared from the circulation on cessation of infusion, and did not reappear in response to posture or isometric exercise. While adrenaline infusion again increased noradrenaline, we found no evidence of subsequent adrenaline release in response to noradrenergic stimulation. These studies do not exclude adrenaline uptake and re-release in amounts sufficient to stimulate the prejunctional beta-adrenoceptor, but insufficient to reach the circulation after local metabolism.