Аннотация:Aim. We studied the mechanisms of hypotension and tachycardia induced by high-dose ethanol (4.5 g/kg body weight, i.p.). Methods. Blood pressure was recorded through a catheter in conscious unrestrained rats and processed beat-to-beat to estimate mean arterial pressure (MAP) and heart rate (HR) values. MAP dynamics was analysed by wavelet decomposition. Vasoconstictor responses of isolated tail artery were studied under constant-flow perfusion. Results. Ethanol administration was followed by a rapid decrease of MAP (by 36±4 mm Hg) and increase of HR (by 48±12 bpm); the changes persisted for 2.5-3 hours. The hypotension was associated with the inhibition of sympathetic vasomotor influences, as judged by: (1) the attenuation of MAP oscillations around 0.4 Hz and (2) two-fold decrease of depressor response to ganglionic blocker chlorisondamine. The tachycardic response to ethanol was due to total depression of vagal tone (the response to methylatropine was absent). Along with that, responses to atenolol did not differ in ethanol-treated and control rats, indicating the absence of ethanol effects on cardiac sympathetic tone. Blood concentration of ethanol 20-60 min after its administration averaged 4.5 mg/ml. In-vitro studies showed that such ethanol concentration did not change the responses of tail artery preparations to electrical field stimulation of sympathetic nerves and to activation of α1-adrenoceptors with phenylephrine. Conclusions. Our data show that high-dose ethanol mainly affects the activity of autonomic nervous system but not peripheral sympathetic neurotransmission or arterial adrenoreactivity. Supported by the Russian Foundation for Basic Research (grant N 13-04-02087).