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Am J Physiol Regul Integr Comp Physiol 279: R1512-R1516, 2000;
0363-6119/00 $5.00
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Vol. 279, Issue 4, R1512-R1516, October 2000

RAPID COMMUNICATION
Angiotensin-converting enzyme inhibitor inhibits dehydration-enhanced fever induced by endotoxin in rats

Tatsuo Watanabe1, Makoto Hashimoto2, Minoru Wada3, Toshiaki Imoto1, Michio Miyoshi1, Daikai Sadamitsu4, and Tsuyoshi Maekawa4

1 Department of Physiology, Tottori University Faculty of Medicine, Yonago, Tottori 683; 2 Department of Otolaryngology and 4 Department of Critical Care and Emergency Medicine, Yamaguchi University School of Medicine, Ube, Yamaguchi 755; and 3 Division of General Education, Tokuyama College of Technology, Tokuyama, Yamaguchi 745, Japan

It has been reported that a host develops a marked fever under dehydrated conditions compared with normally hydrated conditions (11). The present study was carried out to investigate whether ANG II is involved in the enhancement seen in dehydrated rats of the fever induced by bacterial endotoxin. The results showed that intravenous injection of bacterial endotoxin produced a fever in dehydrated rats (rats deprived of water for 24 h) that was significantly greater than that seen in normally hydrated rats. In contrast, dehydration had no effect on the fever induced by intravenous interleukin-1beta (IL-1beta ). Under dehydrated conditions, the enhanced endotoxin-induced fever was significantly inhibited by the angiotensin-converting enzyme inhibitor lisinopril, but the IL-1beta fever was not. These results suggest that the dehydration-induced enhancement of endotoxin fever is due, at least in part, to the action of ANG II, which elicits an increased production of pyrogenic cytokines such as IL-1.

lipopolysaccharide; interleukin-1; pyrogens; febrile response


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