β1‐Adrenoceptors mediate smooth muscle relaxation in mouse isolated trachea

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Abstract
1 The relaxant effects to the β-adrenoceptor agonists isoprenaline, adrenaline, noradrenaline, RO363, procaterol and fenoterol were investigated in carbachol-contracted mouse isolated tracheal preparations. 2 The order of potencies for those β-adrenoceptor agonists that induced full relaxation of carbachol-contracted mouse tracheal preparations was isoprenaline > RO363 > noradrenaline = adrenaline > fenoterol. The EC50 value of isoprenaline for relaxation was 46 nm. The β1-adrenoceptor-selective agonist, RO363, was ten times more potent than the β2-adrenoceptor-selective agonist, fenoterol. The highly β2-adrenoceptor-selective agonist procaterol was a partial relaxant and induced only 28 ± 4% relaxation. 3 Relaxations induced by noradrenaline and isoprenaline were not significantly affected by the neuronal uptake inhibitor, cocaine (10 μm) or by the extraneuronal uptake inhibitor, deoxycorticosterone acetate (25 μm) respectively. The α-adrenoceptor agonist methoxamine induced no observable elevation of mouse tracheal smooth muscle tone. 4 Schild plots for the β-adrenoceptor antagonists, atenolol and betaxolol (β1-adrenoceptor-selective) and ICI 118,551 (β2-adrenoceptor-selective) were linear, with slope values approaching unity. Mean pA2 values derived for atenolol, betaxolol and ICI 118,551 for antagonism of β-adrenoceptor-mediated relaxation were 7.1, 8.4 and 7.2, respectively. These data were independent of the use of isoprenaline or noradrenaline as the agonist. 5 These findings indicate that β-adrenoceptor-mediated relaxations of mouse isolated trachea occur predominantly through activation of β1-adrenoceptors.

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