Administration of L-5-hydroxytryptophan (25 micrograms/kg, s.c.), the immediate precursor of serotonin, to rats induces drinking and increases tail skin temperature. Decreases in both the metabolic rate (rate of oxygen consumption) and colonic temperature also occur. These responses are similar to those observed following acute administration of angiotensin II. However, both drinking and the increase in tail skin temperature are unaffected by prior administration of the non-peptide angiotensin II, AT-1 receptor antagonist, losartan potassium, but are partially attenuated by the beta-adrenoceptor antagonist, propranolol. This suggests that the responses are independent of the angiotensin AT-1 receptor but may be mediated, in part at least, by the beta-adrenoceptor. The hypothesis is presented that when either L-5-hydroxytryptophan or angiotensin II is administered to rats, they act centrally to reduce the set-point for body temperature regulation, thus resulting in the reflex activation of mechanisms that reduce body temperature, including an increase in tail skin temperature and a decrease in metabolic rate.