Functional involvement of alpha 1- and alpha 2-adrenoceptors in 86Rb efflux from liver slices and lipolysis in guinea-pig isolated adipocytes.

1. The application of an alpha 1-adrenoceptor agonist, amidephrine, to guinea-pig liver slices increases glucose release and 86Rb efflux. Since prazosin was more potent than yohimbine in inhibiting both responses, alpha 1-adrenoceptors seem to be involved in the effects evoked by the agonist. 2. Clonidine (an alpha 2-adrenoceptor agonist) at doses unable to activate liver glycogenolysis increased 86Rb release and potentiated isoprenaline in promoting 86Rb efflux. Since yohimbine antagonized clonidine in promoting 86Rb efflux, alpha 2-adrenoceptors also seem to control plasmalemmal permeability to 86Rb. 3. The liver slice responses resulting from alpha 1- and alpha 2-adrenoceptor stimulation required extracellular calcium. Calcium absence or the administration of D-600 attenuated the effects of amidephrine on glucose release and 86Rb outflow and Ca2+ excess re-established both responses. D-600 and apamin blocked clonidine-induced 86Rb efflux, suggesting that alpha 2-adrenoceptor stimulation activates calcium dependent K+ channels. 4. alpha 2-adrenoceptors do not appear to mediate antilipolytic effects in guinea-pig fat cells.