Adrenaline activates in the intact dog a positive feedback loop causing an increase in noradrenaline plasma levels.

Intravenous adrenaline infusions (100 ng . kg-1 min-1) during 30 min resulted in an increase in dog plasma adrenaline and caused a very marked increase in noradrenaline, beginning at 15 min of the infusion and reaching a maximum (10-fold increase) at the end of the infusion. The heart, but not the vascular tissue, showed an increase in adrenaline content. Propranolol (0.5 + 0.5 mg . kg-1) or cocaine (0.5 + 0.5 mg . kg-1) prevented the increase in plasma noradrenaline caused by adrenaline. Isoprenaline (10 ng . kg-1 . min-1) infused during 30 min caused a smaller (2.7-fold) increase in noradrenaline levels, and those effects were also prevented by propranolol or cocaine. From these results, it is concluded that in vivo the increase in noradrenaline plasma levels is due to an activation of beta-adrenoceptors and that this plasma noradrenaline appears to be of neuronal origin. The results also suggest that adrenaline or isoprenaline, after being taken up into nerve terminals, when released activate presynaptic beta-receptors and facilitate the release of neuronal noradrenaline.