Abstract
Overflow of endogenous noradrenaline from rat isolated tracheae was evoked by electrical field stimulation (3 Hz, 540 pulses) in the presence of yohimbine, desipramine and tyrosine. Isoprenaline 100 nmol/l increased the evoked overflow of noradrenaline by about 65%. This effect was antagonized by propranolol (100 nmol/l) and the β2-selective adrenoceptor antagonist ICI 118,551 (100 nmol/l), but not by the β1-selective adrenoceptor antagonist CGP 20712 A (100 nmol/l). The β2-selective adrenoceptor agonist formoterol (1–100 nmol/l) also facilitated the evoked overflow of noradrenaline, but maximally by only about 25% at 10 nmol/l, i.e. formoterol behaved as a partial agonist at these facilitatory β-adrenoceptor. This assumption is also supported by the observation that formoterol (10 nmol/l) acted as antagonist against isoprenaline (100 nmol/l). Mechanical removal of the mucosa resulted in a 30% decrease in tissue noradrenaline and a 55% reduction of the evoked overflow of noradrenaline. In mucosa-denuded preparations isoprenaline failed to facilitate noradrenaline overflow. In the presence of indomethacin (3 μmol/l) the evoked overflow of noradrenaline from mucosa containing preparations was increased by about 50%, but isoprenaline still further facilitated the evoked noradrenaline overflow by about 40%. In conclusion, the overflow of noradrenaline in the rat trachea is facilitated via β2-adrenoceptors, an effect which requires an intact air-way mucosa.
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Correspondence to: K. Racké at the above address
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Brunn, G., Wessler, I., Anderson, G.P. et al. β Adrenoceptor-mediated facilitation of endogenous noradrenaline release from rat isolated trachea. Naunyn-Schmiedeberg's Arch Pharmacol 350, 459–463 (1994). https://doi.org/10.1007/BF00173014
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DOI: https://doi.org/10.1007/BF00173014