SUPPRESSION OF ALCOHOL-INDUCED HYPERTENSION BY DEXAMETHASONE

Background. Alcohol consumption is associated with an increased incidence of hypertension and stroke, but the triggering mechanisms are unclear. In animals, alcohol causes activation of the sympathetic nervous system and also stimulates the release of corticotropin-releasing hormone (CRH), which has sympathoexcitatory effects when administered centrally. Methods. To determine whether alcohol evokes sympathetic activation and whether such activation is attenuated by the inhibition of CRH release, we measured blood pressure, heart rate, and sympathetic-nerve action potentials (using intraneural microelectrodes) in nine normal subjects before and during an intravenous infusion of alcohol (0.5 g per kilogram of body weight over a period of 45 minutes) and for 75 minutes after the infusion. Each subject received two infusions, one after the administration of dexamethasone (2 mg per day) and one after the administration of a placebo for 48 hours. Results. The infusion of alcohol alone evoked a marked (P<0.001) and progressive increase in the mean (+/-SD) rate of sympathetic discharge, from 16+/-3 bursts per minute at base line to 30+/-8 bursts per minute at the end of the two-hour period. This sympathetic activation was accompanied during the second hour by an increase in mean arterial pressure of 10+/-5 mm Hg (P<0.001). After the administration of dexamethasone, the alcohol infusion had no detectable sympathetic effect. The dexamethasone-induced suppression of sympathetic activation was associated with a decrease in mean arterial pressure of 7+/-6 mm Hg (P<0.001) during the alcohol infusion and with suppression of the presser effect during the second hour. Conclusions. Alcohol induces presser effects by sympathetic activation that appear to be centrally mediated. It is possible that these alcohol-induced hemodynamic and sympathetic actions could participate in triggering cardiovascular events.