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α2‐Adrenoceptor blockade prevents cardiac glycoside‐evoked neurotransmitter release from sympathetic nerves in dog saphenous vein

1 The effect of α‐adrenoceptor antagonists upon neurotransmitter release evoked by cardiac glycosides from sympathetic nerve terminals has been investigated in dog saphenous vein. 2 In rings of saphenous vein preloaded with [3H]‐noradrenaline, acetylstrophanthidin (ACS) caused a concentration‐dependent efflux of 3H (EC50 ca. 4.4 μm) that was attenuated by phentolamine and yohimbine but not by prazosin. 3 In helical strips of saphenous vein superfused with ACS at EC50 the efflux of 3H‐compounds in general, and of [3H]‐noradrenaline in particular, occurred after a short delay and increased with time to a maximum reached at 75 min. Phentolamine and phenoxybenzamine, but not prazosin reduced the efflux of [3H]‐noradrenaline and of total 3H‐compounds throughout the time‐course of the ACS‐evoked effect. 4 In helical strips of saphenous vein the glycoside ouabain also caused an increase in [3H]‐noradrenaline and in total 3H‐efflux that was attenuated by phentolamine. 5 By contrast with the above, in bovine adrenal medullary chromaffin cells, which appear to have no functional α‐adrenoceptors, ACS caused a small, but significant increase in 3H‐efflux which was not prevented by phentolamine. 6 Phentolamine, at concentrations that attenuate markedly the ouabain‐or ACS‐evoked increase in 3H‐efflux from dog saphenous vein, did not cause significant inhibition of cocaine‐sensitive [3H]‐noradrenaline uptake nor did it reduce the extent of the 3H‐efflux evoked either by tyramine or by reduced extracellular Na+. These findings imply that phentolamine does not affect ACS‐evoked neurotransmitter release by an action on the catecholamine uptake mechanism. 7 It is concluded that the cardiac glycoside‐evoked increase in neurotransmitter release from noradrenergic nerve terminals of dog saphenous vein is modulated by a mechanism that involves an α2‐adrenoceptor.