Two series of experiments were performed to determine the possible involvement of Ca++ channels in the thermolytic action of ethanol administered at a room temperature of 22 degrees C. In one group of 11 adult female Sprague-Dawley rats, stainless steel guide cannulae were implanted stereotaxically above the lateral cerebral ventricle. Prior to an experiment, a thermistor probe was inserted into the colon so that core temperature could be monitored continuously for up to six hours or until the temperature had returned to a previous baseline level. When the animal's body temperature had stabilized, a dose of 4.0 g/kg in a v/v solution of 20% ethanol was given by intragastric gavage. After the body temperature had declined by about 2.0 degrees C, ordinarily 30 min after ethanol administration, either control CSF or the vehicle plus one of four doses of verapamil (8.3, 25, 50 and 100 micrograms) was infused intracerebroventricularly (ICV) in a volume of 10 microliter. In a second group of 7 unoperated rats, either 4.0 g/kg ethanol or a physiological saline control solution was administered isovolumetrically by intragastric gavage; then, 30 min later, either 3.0 or 10.0 mg/kg verapamil was injected intraperitoneally. At an ambient temperature of 22 degrees C, ethanol gavage produced a significant decline in colonic temperature which was unaffected by physiological saline given by the same route. Although the CSF control vehicle was without effect, verapamil administered ICV attenuated the thermolytic action of ethanol in all doses tested; however, the lowest dose exerted its antagonist effect but with a longer latency. Conversely, when verapamil was given systemically, the hypothermic action of ethanol was significantly potentiated in a dose-dependent manner.(ABSTRACT TRUNCATED AT 250 WORDS)