Beta2-adrenoceptors facilitating noradrenaline secretion from human vasoconstrictor nerves.
Isolated biopsy specimens of human peripheral arteries and veins, preincubated with 3H-(-)- noradrenaline (NA) to label the neural stores of NA, were used to study the Beta-adrenoceptors previously found to increase the secretion of 3H-NA evoked by electrical field stimulation of the adrenergic nerves of this tissue. The increase in nerve stimulation induced secretion of 3H-NA caused by 0.04 muM isoprenaline was prevented by 1 muM propranolol. This beta-blocking drug by itself slightly but significantly depressed the secretion of 3H-NA caused by nerve stimulation in the absence of isoprenaline. While the secretion of 3H-NA was not affected by known beta1-agonists, it was dose-dependently and reversibly increased by two different beta2-agonists. The effect of isoprenaline on 3H-NA secretion was not altered by a selective beta1-antagonist, but strongly reduced or abolished by a beta2-blocking drug. The results indicate that the beta-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 beta2 in nature.
Beta2-adrenoceptors facilitating noradrenaline secretion from human vasoconstrictor nerves. Isolated biopsy specimens of human peripheral arteries and veins, preincubated with 3H-(-)- noradrenaline (NA) to label the neural stores of NA, were used to study the Beta-adrenoceptors previously found to increase the secretion of 3H-NA evoked by electrical field stimulation of the adrenergic nerves of this tissue. The increase in nerve stimulation induced secretion of 3H-NA caused by 0.04 muM isoprenaline was prevented by 1 muM propranolol. This beta-blocking drug by itself slightly but significantly depressed the secretion of 3H-NA caused by nerve stimulation in the absence of isoprenaline. While the secretion of 3H-NA was not affected by known beta1-agonists, it was dose-dependently and reversibly increased by two different beta2-agonists. The effect of isoprenaline on 3H-NA secretion was not altered by a selective beta1-antagonist, but strongly reduced or abolished by a beta2-blocking drug. The results indicate that the beta-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 beta2 in nature.