Inhibition by ethanol of noradrenaline output from peripheral sympathetic nerves: possible interaction of ethanol with neuronal receptors.

The sympathetic nerve terminals of the isolated rabbit heart perfused with Tyrode solution were used to study the action of ethanol on the noradrenaline uptake and release. The uptake of exogenous noradrenaline (10 ng/ml) into the sympathetic nerve endings, the noradrenaline output evoked by raising the concentration of potassium ions in the perfusion fluid, and the release in response to electrical stimulation of the nerve axons were inhibited only by lethal concentrations of the alcohol; the concentrations which caused 50% inhibition (IC50) amounted to 760 mM, 830mM, and 1150 mM respectively. However, ethanol at concentrations compatible with moderate intoxication reduced the noradrenaline release in response to activation of the nicotine receptors on the nerve terminals by dimethylphenylpiperazine; the threshold concentration was 36 mM and the IC50 was 129 mM. It is suggested that this effect is due to hydrophobic interaction of the alcohol with receptor proteins, thus inhibiting stimulus formation.