Arginine vasopressin in fever: a still unsolved puzzle

(1) Administration of arginine vasopressin (AVP) in the ventral septal area (VSA) or intracerebroventricularly (i.c.v.) is thought to attenuate lipopolysaccharide (LPS) or prostaglandin (PG) E 2 fevers in rabbits and rats by acting on the V 1 receptor. (2) We found that the fever response of rabbits to intravenous LPS (200 ng/kg) or intra-VSA PGE 2 (500 ng) was not attenuated but enhanced by intra-VSA AVP (5 μg); a pharmacological analysis showed that this fever-enhancing effect was mediated by the V 2 receptor. (3) The febrile response of rats to intraperitoneal (50 μg/kg) or i.c.v. (100 ng) LPS was unaffected by i.c.v. AVP (2.5–100 ng). (4) The role of AVP in fever should be re-examined.