PMID- 9262354
OWN - NLM
STAT- MEDLINE
DCOM- 19970911
LR  - 20131121
IS  - 0022-3565 (Print)
IS  - 0022-3565 (Linking)
VI  - 282
IP  - 2
DP  - 1997 Aug
TI  - The effect of central angiotensin II receptor blockade on interleukin-1beta- and 
      prostaglandin E-induced fevers in rats: possible involvement of brain angiotensin 
      II receptor in fever induction.
PG  - 873-81
AB  - We investigated the role of the brain angiotensin II (Ang II) receptor subtypes 
      AT1 and AT2 in the development of fever induced in freely moving rats by 
      administration of interleukin-1beta (IL-1beta) or prostaglandin E2 (PGE2). 
      Intraperitoneal (i.p.) injection of IL-1beta (2 microg/kg) induced a marked fever 
      of rapid onset. Intracerebroventricular (i.c.v.) administration, immediately 
      before IL-1beta injection, of a selective AT2 receptor antagonist, CGP42112A (5 
      or 20 microg), reduced the fever in a dose-related manner. Rats given an i.c.v. 
      injection of PGE2 (200 ng) developed a monophasic fever response that was 
      attenuated by i.c.v. treatment with CGP42112A (10 or 20 microg) in a dose-related 
      manner. The IL-1beta (2 microg/kg i.p.)- and PGE2 (200 ng i.c.v.)-induced fevers 
      were unchanged by the selective AT1 receptor antagonist losartan (60 microg 
      i.c.v.). Treatment with exogenous Ang II (100 ng i.c.v.), which itself had no 
      effect on resting body temperature, resulted in an enhancement of the PGE2 (50 ng 
      i.c.v.)-induced fever. The administration of CGP42112A (2 and 5 microg) into the 
      rostral hypothalamus (preoptic/anterior hypothalamic region) reduced fevers 
      induced by IL-1beta (2 microg/kg i.p.) or intrahypothalamic (i.h.) PGE2 (100 ng). 
      Moreover, i.h. injection of Ang II (25 ng) augmented the PGE2 (25 ng 
      i.h.)-induced fever. Finally, the i.h. administration, 15 min before i.h. PGE2 
      (100 ng), of the angiotensin-converting enzyme (ACE) inhibitor lisinopril (5 and 
      10 microg) attenuated the PGE2-induced fever. These results suggest that brain 
      AT2 receptors contribute to the induction of such febrile responses in rats.
FAU - Watanabe, T
AU  - Watanabe T
AD  - The Department of Physiology, Yamaguchi University School of Medicine, Ube, 
      Japan.
FAU - Saiki, Y
AU  - Saiki Y
FAU - Sakata, Y
AU  - Sakata Y
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Pharmacol Exp Ther
JT  - The Journal of pharmacology and experimental therapeutics
JID - 0376362
RN  - 0 (Angiotensin Receptor Antagonists)
RN  - 0 (Interleukin-1)
RN  - 0 (Receptors, Angiotensin)
RN  - 11128-99-7 (Angiotensin II)
RN  - K7Q1JQR04M (Dinoprostone)
SB  - IM
MH  - Angiotensin II/*metabolism
MH  - *Angiotensin Receptor Antagonists
MH  - Animals
MH  - Brain/*drug effects/metabolism
MH  - Dinoprostone/antagonists & inhibitors/*toxicity
MH  - Fever/*chemically induced
MH  - Hypothalamus
MH  - Injections, Intraventricular
MH  - Interleukin-1/antagonists & inhibitors/*toxicity
MH  - Male
MH  - Rats
MH  - Rats, Wistar
MH  - Receptors, Angiotensin/physiology
EDAT- 1997/08/01 00:00
MHDA- 1997/08/01 00:01
CRDT- 1997/08/01 00:00
PHST- 1997/08/01 00:00 [pubmed]
PHST- 1997/08/01 00:01 [medline]
PHST- 1997/08/01 00:00 [entrez]
PST - ppublish
SO  - J Pharmacol Exp Ther. 1997 Aug;282(2):873-81.