Abstract
1 Depolarizations of freshly-dissected isolated superior cervical ganglia of the rat were recorded extracellularly. The following sympathomimetic amines (in order of decreasing potency) produced depolarizations of up to 0.4 mV: isoprenaline, salbutamol, adrenaline, noradrenaline. Depolarizations were lost after overnight storage, leaving only hyperpolarizing responses. 2 Depolarizations by isoprenaline were antagonized by (-)-propranolol (pA2 8.94 ± 0.15), (±)-butoxamine (pA2 7.36 ± 0.12) and (±)-practolol (pA2 5.14 ± 0.13). They were not blocked by phentolamine (1 μm) or phenoxybenzamine (1 μm). Isoprenaline and salbutamol were antagonized with equal facility by practolol or butoxamine. 3 In concentrations producing ganglionic depolarization, these compounds also produced a smaller depolarization of presynaptic elements in the ganglion, but not preganglionic trunk fibres. Presynapic depolarization was blocked by 100 nM propranolol but not by 1 μm phentolamine. 4 Isoprenaline and salbutamol increased the amplitude of the compound ganglionic action potential recorded following single preganglionic nerve stimuli when transmission had been rendered submaximal by adjusting the Ca/Mg ratio, but not in normal solution. 5 Isoprenaline (0.1 μm) also increased the amount of [3H]-acetylcholine released by preganglionic stimulation in low Ca/high Mg solution. 6 It is concluded that facilitatory adrenoceptors are present on pre- and postsynaptic elements in rat superior cervical ganglia, which resembles the ‘β2’ subclass of β-receptors.