PMID- 10425188
OWN - NLM
STAT- MEDLINE
DCOM- 19990908
LR  - 20141120
IS  - 0006-291X (Print)
IS  - 0006-291X (Linking)
VI  - 261
IP  - 2
DP  - 1999 Aug 2
TI  - Increased vasoconstrictor response of the mouse lacking angiotensin II type 2
      receptor.
PG  - 345-9
AB  - The angiotensin II (Ang II) type 1 receptor mediates various actions of Ang II,
      whereas the function of the type 2 (AT2) receptor is not well understood. In the 
      mice lacking the gene encoding the AT2 receptor, the pressor response to Ang II
      was increased although the underlying mechanism is unknown. We tested the
      hypothesis that vasoconstrictor response is exaggerated in the AT2 receptor null 
      mice. We measured hemodynamic parameters and evaluated systemic vascular
      resistance (SVR) in the anesthetized open-chest wild-type and AT2 receptor null
      mice. Ang II infusion caused dose-dependent increases in SVR in both strains,
      while the response was significantly higher at 0.5 microgram/kg Ang II in the AT2
      receptor null mice (305 +/- 53% of baseline) than in the wild-type mice (179 +/- 
      27% of baseline). To investigate further the vascular contractility, we examined 
      contraction of aortic rings in vitro. The contraction induced by 1 microM Ang II 
      was increased in the AT2 receptor null mice compared with that in the wild-type
      mice (0.82 +/- 0.11 vs. 0.54 +/- 0.12 g). Ang II-induced contraction was still
      greater in the AT2 receptor null mice when calibrated by the maximum tension
      induced by 90 mM KCl. These data suggest that the AT2 receptor modulates vascular
      contractility, which may influence blood pressure.
CI  - Copyright 1999 Academic Press.
FAU - Akishita, M
AU  - Akishita M
AD  - Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, 75 
      Francis Street, Boston, Massachusetts, 02115, USA.
FAU - Yamada, H
AU  - Yamada H
FAU - Dzau, V J
AU  - Dzau VJ
FAU - Horiuchi, M
AU  - Horiuchi M
LA  - eng
GR  - HL35252/HL/NHLBI NIH HHS/United States
GR  - HL35610/HL/NHLBI NIH HHS/United States
GR  - HL46631/HL/NHLBI NIH HHS/United States
GR  - etc.
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Biochem Biophys Res Commun
JT  - Biochemical and biophysical research communications
JID - 0372516
RN  - 0 (Receptor, Angiotensin, Type 2)
RN  - 0 (Receptors, Angiotensin)
RN  - 11128-99-7 (Angiotensin II)
SB  - IM
MH  - Angiotensin II/pharmacology
MH  - Animals
MH  - Aorta, Thoracic/drug effects/physiology
MH  - Blood Pressure/drug effects
MH  - Hemodynamics/drug effects
MH  - In Vitro Techniques
MH  - Male
MH  - Mice
MH  - Mice, Knockout
MH  - Receptor, Angiotensin, Type 2
MH  - Receptors, Angiotensin/deficiency/genetics/*physiology
MH  - Vascular Resistance/drug effects
MH  - Vasoconstriction/drug effects/genetics/*physiology
EDAT- 1999/07/30 00:00
MHDA- 1999/07/30 00:01
CRDT- 1999/07/30 00:00
PHST- 1999/07/30 00:00 [pubmed]
PHST- 1999/07/30 00:01 [medline]
PHST- 1999/07/30 00:00 [entrez]
AID - 10.1006/bbrc.1999.1027 [doi]
AID - S0006-291X(99)91027-6 [pii]
PST - ppublish
SO  - Biochem Biophys Res Commun. 1999 Aug 2;261(2):345-9. doi: 10.1006/bbrc.1999.1027.