Prejunctional β2‐adrenoreceptor blockade reduces nerve stimulation evoked release of endogenous noradrenaline in skeletal musclein situ

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Abstract
Prejunctional β‐adrenoceptor‐mediated modulation of endogenous noradrenaline (NA) overflow elicited by sympathetic nerve stimulation was studied in blood‐perfused canine gracilis musclein situ.An attempt was made to subclassify these β‐adrenoceptors by comparing the effects of β1‐selective (metoprolol) and non‐selective (propranolol) β‐adrenoceptor blockade. Animals were pre‐treated with desipramine and phenoxybenzamine in order to counteract possible influences of neuronal uptake and stimulation‐evoked changes in vascular resistance on the diffusion of NA into the blood stream. Metoprolol did not decrease stimulation‐evoked NA overflow, as compared with control experiments (−10 and −8 %, respectively). However, propranolol reduced stimulation‐evoked NA overflow by 30% in metoprolol pre‐treated animals (P< 0.05vs.control experiments). Both antagonists elevated basal perfusion pressure, suggesting that vascular post‐junctional β1‐as well as β2‐adrenoceptors are present. Propranolol increased stimulation‐evoked vasoconstriction in metoprolol pre‐treated animals, indicating that neuronally released NA may activate postjunctional β2‐adrenoceptors under these experimental conditions. In conclusion, our findings suggest that NA release can be enhanced by activation of prejunctional β2‐adrenoceptorsin vivo.