Effects of selective α 2 ‐adrenergic receptor agonists on electrical field‐stimulated contractions of isolated bronchi in horses

We investigated the effects of different selective α 2 ‐adrenergic receptor ( AR ) agonists (detomidine, medetomidine, xylazine, and brimonidine) on the contractions of horse‐isolated bronchi induced by electrical field stimulation ( EFS ) and by carbachol. No effects were observed on the contraction induced by carbachol, while α 2 ‐ AR agonists reduced EFS ‐evoked contractions in a concentration‐related fashion. The rank order of potency ( pD 2 ) was brimonidine (7.40 ± 0.20) >medetomidine (7.09 ± 0.24) >detomidine (6.13 ± 0.55) >xylazine (4.59 ± 0.16). The maximal effects (E max ) were −56.3% ± 6.3%, −40.4% ± 6.9%, −48.6% ± 9.9%, and −72.7% ± 12.7% for brimonidine, medetomidine, detomidine, and xylazine, respectively. Adrenergic block by guanethidine enhanced the potency (8.10 ± 0.05, 7.30 ± 0.15, 6.83 ± 0.41, and 5.40 ± 0.22) and the efficacy (−95.2% ± 0.7%, −45.2% ± 11.7%, −58.5% ± 9.8%, and −97.9% ± 0.6%) of brimonidine, medetomidine, detomidine, and xylazine, respectively. Selective α 2 ‐ AR antagonist, atipamezole, competitively antagonized the inhibition of EFS ‐evoked contractions induced by all agonists except xylazine. These results suggest the existence of presynaptic α 2 ‐ AR s on cholinergic neurons, negatively regulating the release of acetylcholine in horse bronchial muscle, and that α 2 ‐ AR agonists may be beneficial against vagally mediated bronchoconstriction.