PMID- 16677737
OWN - NLM
STAT- MEDLINE
DCOM- 20061107
LR  - 20131121
IS  - 0196-9781 (Print)
IS  - 0196-9781 (Linking)
VI  - 27
IP  - 9
DP  - 2006 Sep
TI  - Effects of i.c.v. losartan on the angiotensin II-mediated vasopressin release and 
      hypothalamic fos expression in near-term ovine fetuses.
PG  - 2230-8
AB  - Our previous studies have shown that central administration of angiotensin (ANG 
      II) causes arginine vasopressin (AVP) release in the fetus at 70-90% gestation. 
      This is evidence that the hypothalamic-neurohypophysial system is relatively 
      mature before birth. However, few data exist regarding central ANG receptor 
      mechanisms-mediated AVP response during fetal life. To determine roles of brain 
      ANG receptor subtypes in this response, AT1 and AT2 receptor antagonists, 
      losartan and PD123319, were investigated in the brain in chronically prepared 
      ovine fetuses at the last third of gestation. Application of losartan 
      intracerebroventricularly (i.c.v.) at 0.5 mg/kg suppressed central ANG 
      II-stimulated plasma AVP release. Losartan at 5 mg/kg (i.c.v.) demonstrated a 
      significant enhancement of AVP increase to i.c.v. ANG II. Associated with the 
      increase of plasma vasopressin levels, c-fos expression in the hypothalamic 
      neurons was significantly different between the low and high doses of losartan. 
      The low dose losartan markedly reduced the dual immunoreactivity for FOS and AVP 
      in the supraoptic nuclei and paraventricular nuclei after i.c.v. ANG II, whereas 
      the high dose losartan together with ANG II, significantly increased the 
      co-localization of positive FOS in the AVP-containing neurons than that induced 
      by i.c.v. ANG II alone. Central ANG II induced fetal plasma vasopressin increase 
      was not altered by PD123319. The data suggest that losartan in the fetal brain 
      has remarkably different effects based on the doses administrated on central ANG 
      II-related neuroendocrine effects at the late gestation, and that the AT1 
      mechanism is critical in the regulation of fetal body fluid homeostasis related 
      to plasma AVP levels.
FAU - Shi, Lijun
AU  - Shi L
AD  - Department of Human Sport Science, Beijing Sport University, Beijing 100084, 
      China.
FAU - Mao, Caiping
AU  - Mao C
FAU - Wu, Jiawei
AU  - Wu J
FAU - Morrissey, Paul
AU  - Morrissey P
FAU - Lee, Juanxiu
AU  - Lee J
FAU - Xu, Zhice
AU  - Xu Z
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20060504
PL  - United States
TA  - Peptides
JT  - Peptides
JID - 8008690
RN  - 0 (Imidazoles)
RN  - 0 (Proto-Oncogene Proteins c-fos)
RN  - 0 (Pyridines)
RN  - 11000-17-2 (Vasopressins)
RN  - 11128-99-7 (Angiotensin II)
RN  - 113-79-1 (Arginine Vasopressin)
RN  - 130663-39-7 (PD 123319)
RN  - JMS50MPO89 (Losartan)
SB  - IM
MH  - Angiotensin II/*antagonists & inhibitors
MH  - Animals
MH  - Arginine Vasopressin/*blood/metabolism
MH  - Female
MH  - Fetus/cytology/*metabolism
MH  - Hypothalamus/cytology/drug effects/*metabolism
MH  - Imidazoles/metabolism/pharmacology
MH  - Injections, Intraventricular
MH  - Losartan/administration & dosage/*pharmacology
MH  - Pregnancy
MH  - Proto-Oncogene Proteins c-fos/*metabolism
MH  - Pyridines/metabolism/pharmacology
MH  - Sheep
MH  - Time Factors
MH  - Vasopressins/*metabolism
EDAT- 2006/05/09 09:00
MHDA- 2006/11/09 09:00
CRDT- 2006/05/09 09:00
PHST- 2006/01/16 00:00 [received]
PHST- 2006/03/14 00:00 [revised]
PHST- 2006/03/14 00:00 [accepted]
PHST- 2006/05/09 09:00 [pubmed]
PHST- 2006/11/09 09:00 [medline]
PHST- 2006/05/09 09:00 [entrez]
AID - S0196-9781(06)00121-5 [pii]
AID - 10.1016/j.peptides.2006.03.013 [doi]
PST - ppublish
SO  - Peptides. 2006 Sep;27(9):2230-8. doi: 10.1016/j.peptides.2006.03.013. Epub 2006 
      May 4.