β₂‐Adrenoceptors Facilitating Noradrenaline Secretion from Human Vasoconstrictor Nerves

Abstract

Abstract Isolated superfused biopsy specimens of human peripheral arteries and veins, preincubated with 3 H‐(‐)‐noradrenaline (NA) to label the neural stores of NA, were used to study the β‐adrenoceptors previously found to increase the secretion of 3 H‐NA evoked by electrical field stimulation of the adrenergic nerves of this tissue. The increase in nerve stimulation induced secretion of 3 H‐NA caused by 0.04μM isoprenaline was prevented by 1 μM propranolol. This &bT‐blocking drug by itself slightly but significantly depressed the secretion of 3 H‐NA caused by nerve stimulation in the absence of isoprenaline. While the secretion of 3 H‐NA was not affected by two known β 1 ‐agonists, it was dose‐dependently and reversibly increased by two different β 2 ‐agonists. The effect of isoprenaline on 3 H‐NA secretion was not altered by a selective β‐antagonist, but strongly reduced or abolished by a β 2 ‐blocking drug. The results indicate that the β‐adrenoceptors involved in the control of NA secretion from the vasoconstrictor nerves of human omental blood vessels are only to a minimal extent stimulated by NA secreted from the nerves, and therefore do probably not mainly serve to mediate local positive feedback control of transmitter secretion; the receptors appear to be β 2 in nature.