Facilitatory prejunctional beta-adrenoceptors in human arteries and veins

The effects of beta-adrenoceptor agonists and antagonists on both the transmitter outflow and the associated pressure response produced by perivascular nerve stimulation have been studied in human digital arteries and metatarsal veins, in which transmitter stores were labelled with [3H]noradrenaline. Both isoprenaline in arteries, and salbutamol in arteries and veins, at concentrations of 10(-8) - 10(-6) mol/l significantly enhanced stimulation-induced tritium outflow. These two agonists were approximately equipotent. Salbutamol also potentiated pressure responses to stimulation, and propranolol prevented the enhancement of stimulation-induced tritium outflow by salbutamol. Adrenaline, at a concentration of 10(-8) mol/l, but not lower concentrations, significantly enhanced stimulation-induced tritium outflow in arteries. Propranolol, however, had no effect on stimulation-induced transmitter outflow, even when the arteries were either perfused throughout the experiment with a low concentration of adrenaline, or when the arteries were preincubated in a high concentration of adrenaline as well as perfused throughout with a low concentration of adrenaline. It is concluded that facilitatory prejunctional beta-adrenoceptors (probably of the beta 2-subtype) are present in human arteries and veins, but that under the conditions of these experiments, neither transmitter noradrenaline, nor adrenaline that has been incorporated into transmitter stores with noradrenaline, activate these prejunctional beta-adrenoceptors. They may, however, be activated under conditions of enhanced adrenomedullary secretion.