Intravenous administration of a bolus of ethanol (40 mg/100 g b.w.) to rats induced bradycardia, hypotension and apnea. Bradycardia was dose dependent (r = -0.78, p less than 0.001). Acute bilateral vagotomy blocked bradycardia and hypotension. Apnea, however, persisted in all cases but was of short duration and occurred after a significant delay as compared to an untreated group. Atropine (0.1 mg/100 g b.w.) and hexamethonium (0.75 mg/100 g b.w.) blocked bradycardia and early hypotension. Pretreatment with reserpine (0.25 mg/100 g b.w. IP 24 and 48 hours before the experiment) significantly increased bradycardia induced by ethanol as compared to untreated animals. In rats pretreated with reserpine and vagotomized, IV ethanol did not induce bradycardia, early hypotension or apnea. A bolus of ethanol (20 mg/100 g b.w.) given directly into the left ventricle did not induce reflex changes in heart rate or respiration, while the same dose of alcohol given IV decreased heart rate by 53 +/- 8.9%. Thus, the ethanol effect seems to be initiated in pulmonary J receptors. Bradycardia appeared to be mediated both by increase in vagal tone, and to a lesser extent, by sympathetic withdrawal. Hypotension was due mainly to bradycardia, and apnea might be caused by a dual mechanism, reflex (early) and direct on the respiratory center (late).