PMID- 15342270
OWN - NLM
STAT- MEDLINE
DCOM- 20041223
LR  - 20171208
IS  - 0006-8993 (Print)
IS  - 0006-8993 (Linking)
VI  - 1021
IP  - 2
DP  - 2004 Sep 24
TI  - Pressor response to CSF sodium in mice: mediation by a ouabain-like substance and 
      renin-angiotensin system in the brain.
PG  - 219-31
AB  - Intracerebroventricular (i.c.v.) infusion of sodium in rats increases 
      cerebrospinal fluid (CSF) [Na], mimicking the effects of a high salt diet in 
      salt-sensitive strains and causing sympathetic hyperactivity and a pressor 
      response that are mediated via both an endogenous brain ouabainlike substance 
      (OLS) and the brain renin-angiotensin system (RAS). However, the concept that CSF 
      sodium activates both the brain OLS and brain RAS to increase blood pressure has 
      not been tested in any other species besides the rat. In the current study, it 
      was established that continuous i.c.v. infusion of NaCl causes sustained 
      increases in blood pressure and heart rate in both outbred (Swiss Webster, SW) 
      and inbred (C57Bl/6) mouse strains. Subsequently, the mechanisms of the pressor 
      effects were explored. In both SW and C57Bl/6, the i.c.v. administration of Fab 
      fragments of an antibody with high affinity for ouabain and the OLS (Fab) 
      abolished the pressor and tachycardic responses to i.c.v. sodium, as did the 
      angiotensin II AT1 receptor antagonist losartan given i.c.v. In contrast, doses 
      of NaCl, Fab and losartan that were effective i.c.v. were ineffective when given 
      i.v. I.c.v. ouabain also caused the pressor and tachycardic responses, which were 
      abolished by losartan (i.c.v.). In the reciprocal study, i.c.v. Fab had no effect 
      on similar responses to i.c.v. angiotensin II. These studies demonstrate that the 
      sustained blood pressure and heart rate responses caused by increases in CSF [Na] 
      are mediated via both a brain OLS and the brain RAS. The RAS activation occurs 
      downstream of the OLS effect.
FAU - Van Huysse, James W
AU  - Van Huysse JW
AD  - Hypertension Unit, University of Ottawa Heart Institute, Room H-347, 40 Ruskin 
      Street, Ottawa, Ontario, Canada K1Y 4W7. jvanhuysse@ottawaheart.ca
FAU - Hou, Xiaohong
AU  - Hou X
LA  - eng
GR  - 32435-1/Canadian Institutes of Health Research/Canada
GR  - 74572-1/Canadian Institutes of Health Research/Canada
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Netherlands
TA  - Brain Res
JT  - Brain research
JID - 0045503
RN  - 0 (Antihypertensive Agents)
RN  - 0 (Cardiotonic Agents)
RN  - 0 (Immunoglobulin Fab Fragments)
RN  - 11128-99-7 (Angiotensin II)
RN  - 451W47IQ8X (Sodium Chloride)
RN  - 5ACL011P69 (Ouabain)
RN  - 9NEZ333N27 (Sodium)
RN  - JMS50MPO89 (Losartan)
SB  - IM
MH  - Angiotensin II/pharmacology
MH  - Animals
MH  - Antihypertensive Agents/pharmacology
MH  - Blood Pressure/drug effects
MH  - Cardiotonic Agents/*metabolism
MH  - Heart Rate/drug effects
MH  - Humans
MH  - Immunoglobulin Fab Fragments/pharmacology
MH  - Injections, Intraventricular
MH  - Losartan/pharmacology
MH  - Male
MH  - Mice
MH  - Ouabain/metabolism
MH  - Renin-Angiotensin System/*drug effects/*physiology
MH  - Sodium/*cerebrospinal fluid/metabolism/pharmacology
MH  - Sodium Chloride/*administration & dosage
EDAT- 2004/09/03 05:00
MHDA- 2004/12/24 09:00
CRDT- 2004/09/03 05:00
PHST- 2004/06/28 00:00 [accepted]
PHST- 2004/09/03 05:00 [pubmed]
PHST- 2004/12/24 09:00 [medline]
PHST- 2004/09/03 05:00 [entrez]
AID - S0006-8993(04)01070-4 [pii]
AID - 10.1016/j.brainres.2004.06.056 [doi]
PST - ppublish
SO  - Brain Res. 2004 Sep 24;1021(2):219-31. doi: 10.1016/j.brainres.2004.06.056.