Relaxation of cat trachea by β-adrenoceptor agonists can be mediated by both β1- and β2-adrenoceptors and potentiated by inhibitors of extraneuronal uptake

Responses (relaxation) to the β‐adrenoceptor agonists, isoprenaline, fenoterol or noradrenaline, were obtained on cat tracheal preparations contracted with a submaximal concentration of carbachol (0.5 μm). The relative potencies of isoprenaline: fenoterol: noradrenaline were 100:8.1:10.7. From this, it was concluded that responses were mediated predominantly by β‐adrenoceptors but that a minor population of β‐adrenoceptors might also be involved. Schild plots for the selective antagonists atenolol (β‐selective) or ICI 118, 551 (β‐selective) were in different locations, i.e. were separated, depending on whether the antagonist was antagonizing noradrenaline or fenoterol. This supported the conclusion that β‐ as well as β‐adrenoceptors were involved in mediating the response. In this respect, cat trachea resembles cat atria (rate responses). In the presence of atenolol the concentration‐response curves to fenoterol became biphasic. This was interpreted as indicating that the β‐adrenoceptors were too few in number to elicit a maximum tissue response. Responses to isoprenaline of cat trachea were potentiated by the extraneuronal uptake inhibitor drugs, corticosterone and metanephrine. This indicated that extraneuronal uptake could modulate β‐adrenoceptor‐mediated responses (relaxation) of cat trachea. Cat trachea resembles guinea‐pig trachea in that (i) the β‐adrenoceptor population mediating relaxation is mixed (β + β) and (ii) responses to isoprenaline are modulated by its extraneuronal uptake. However, cat trachea differs from guinea‐pig trachea in that the predominant β‐adrenoceptor sub‐type is β not β. 1983 British Pharmacological Societ