Modulation of transmission in rat sympathetic ganglia by activation of presynaptic alpha- and beta-adrenoceptors.

1 Conditions under which transmission in rat isolated superior cervical ganglia may be affected by activation of presynaptic alpha- and beta-adrenoceptors have been investigated by means of an extracellular recording method. 2 Clonidine caused a small hyperpolarization of the ganglia (mean EC50 approximately 2 nM) in unstimulated preparations; with continuous preganglionic stimulation at 0.2 Hz, clonidine markedly decreased the height of the compound action potential (mean EC50 approximately 18 nM). 3 Phentolamine (0.1-3 microM) per se increased the height of the compound action potential by up to 15%, and antagonized the inhibitory effects of adrenaline and clonidine. 4 Using a higher frequency of stimulation (0.5 Hz), the effect of phentolamine (1 microM) was unchanged, whereas the inhibitory effectiveness of adrenaline on the height of the compound action potential was reduced. 5 (+/-)-Propranolol (0.1 microM) did not affect the height of the compound action potential, whereas the inhibitory effects of high concentrations of adrenaline were enhanced. 6 During an infusion of clonidine (1 microM), adrenaline (1-100 microM) and, less effectively, noradrenaline (10-100 microM) increased the height of the compound action potential by up to 14%; these effects were antagonized by propranolol (0.1 microM). 7 In the presence of noradrenaline (10 and 30 microM) adrenaline (100 microM) caused a small (up to 5%) enhancement of the height of the compound action potential. 8 The results obtained are consistent with the existence of presynaptic alpha- and beta-adrenoceptors on preganglionic terminals. The alpha-adrenoceptor may be part of a trans-synaptic inhibitory feedback. mechanism; however the functional role of the facilitatory beta-adrenoceptor is not clear.