Cyclic adenosine 3′,5′-monophosphate and β-effects in rat isolated superior cervical ganglia

Abstract

1 Isoprenaline (0.01–1 μm) increased the amount of cyclic adrenosine 3′,5′-monophosphate (cyclic AMP) in rat isolated superior cervical ganglia by up to 10 times after 10 min application. Cyclic AMP levels returned to control values after 20 min washing. 2 Salbutamol, in concentrations (1–100 μm) that depolarized the ganglion and facilitated submaximal transmission, did not significantly raise ganglionic cyclic AMP levels. 3 The action of isoprenaline was antagonized by butoxamine (apparent K_I≅0.14 μm) and weakly by practolol (apparent K_I≅9.1 μm). 4 The effect of 0.1 μm isoprenaline was also inhibited 94% by 100 μm of the adenylate cyclase inhibitor, 9-(tetrahydro-2-furyl)adenine (SQ 22,536). 5 Exogenous dibutyryl cyclic AMP did not replicate the effects of isoprenaline on ganglionic d.c. potentials or submaximal transmission. 6 The phosphodiesterase inhibitors theophylline, isobutylmethylxanthine or 4-(3,4-dibutoxybenzyl)-2-imidazolidinone (Ro 20–1724) did not potentiate these electrical responses to isoprenaline. 7 The adenylate cyclase inhibitor, SQ 22,536, did not inhibit the electrical responses to isoprenaline. 8 It is concluded that available evidence does not support the view that the ganglion depolarization or facilitation of submaximal transmission in rat isolated ganglia produced by isoprenaline are likely to be mediated by cyclic AMP.