Prejunctional beta-adrenoceptors in human digital arteries.

Abstract

The effects of β-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, in which transmitter stores were labelled with [3H]noradrenaline. Both isoprenaline and salbutamol 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. Adrenaline, at a concentration of 10−8 mol/l, but not lower concentrations, produced a significant enhancement of the stimulation-induced tritium outflow which was associated with a small, but non-significant, potentiation of the pressure response to stimulation. Propranolol prevented the enhancement of stimulation-induced tritium outflow by salbutamol 10−7 mol/l and adrenaline 10−8 mol. Dobutamine 10−7 mol/l, but not 10−8 mol/l, significantly enhanced stimulation-induced tritium outflow. Resting outflow was markedly increased by higher concentrations of dobutamine. No potentiation of pressure responses to stimulation was produced by dobutamine. Propranolol and metoprolol had no effect on stimulation-induced transmitter outflow. Propranolol also had no effect on stimulation-induced outflow when the arteries were either perfused throughout the experiment with a low concentration of adrenaline or salbutamol, or when the arteries were preincubated in a high concentration of adrenaline as well as perfused throughout with a low concentration of adrenaline. Resting and stimulation-induced tritium outflow from arteries incubated in [3H]adrenaline was much lower and more variable than the outflow from arteries incubated in [3H]noradrenaline. It is concluded that facilitatory prejunctional β-adrenoceptors (probably of the β2-subtype) are present in human digital arteries, 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 β-adrenoceptors.