PMID- 7536713
OWN - NLM
STAT- MEDLINE
DCOM- 19950525
LR  - 20190722
IS  - 0194-911X (Print)
IS  - 0194-911X (Linking)
VI  - 25
IP  - 4 Pt 2
DP  - 1995 Apr
TI  - Relaxation of the aorta during hypoxia is impaired in chronically hypertensive 
      rats.
PG  - 735-8
AB  - We investigated mechanisms by which hypoxia produces relaxation of the aorta and 
      tested the hypothesis that these mechanisms are altered during chronic 
      hypertension. Tension of thoracic aortae from normotensive Wistar-Kyoto (WKY) 
      rats and stroke-prone spontaneously hypertensive rats (SHRSP) was measured in an 
      organ bath under control conditions and at two levels of hypoxia. In WKY rats, 
      mild and severe hypoxia produced relaxation of the aortae (precontracted with 
      phenylephrine) by 33 +/- 4% and 82 +/- 3%, respectively (mean +/- SEM). Removal 
      of endothelium or administration of NG-nitro-L-arginine (10(-4) mol/L), an 
      inhibitor of nitric oxide synthase, abolished relaxation of the aortae in 
      response to mild hypoxia but did not affect relaxation during severe hypoxia. 
      Glibenclamide (10(-6) mol/L), an inhibitor of potassium channels, attenuated 
      relaxation of the aortae during mild and severe hypoxia by 49 +/- 16% and 74 +/- 
      4%, respectively. In SHRSP, mild hypoxia produced little relaxation of the aortae 
      (3 +/- 4%, P < .05 compared with WKY). Indomethacin did not increase relaxation 
      to mild hypoxia in SHRSP, which suggests that a cyclooxygenase-derived 
      contracting factor does not contribute to impaired relaxation. Severe hypoxia 
      relaxed the aortae by 86 +/- 4% in SHRSP, and glibenclamide inhibited this 
      response by 60 +/- 9%. These findings suggest that relaxation of the aorta in 
      response to mild hypoxia in WKY rats is mediated primarily by endothelium-derived 
      relaxing factor, and the response to mild hypoxia is markedly impaired in 
      SHRSP.(ABSTRACT TRUNCATED AT 250 WORDS)
FAU - Taguchi, H
AU  - Taguchi H
AD  - Department of Internal Medicine, University of Iowa College of Medicine, Iowa 
      City 52242, USA.
FAU - Faraci, F M
AU  - Faraci FM
FAU - Kitazono, T
AU  - Kitazono T
FAU - Heistad, D D
AU  - Heistad DD
LA  - eng
GR  - AG-10269/AG/NIA NIH HHS/United States
GR  - HL-16066/HL/NHLBI NIH HHS/United States
GR  - NS-24621/NS/NINDS NIH HHS/United States
GR  - etc.
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Hypertension
JT  - Hypertension (Dallas, Tex. : 1979)
JID - 7906255
RN  - 0 (Potassium Channel Blockers)
RN  - 0 (Scorpion Venoms)
RN  - 115422-61-2 (Charybdotoxin)
RN  - 169D1260KM (Nitroprusside)
RN  - SX6K58TVWC (Glyburide)
SB  - IM
MH  - Animals
MH  - Aorta/*physiopathology
MH  - Charybdotoxin
MH  - Chronic Disease
MH  - Glyburide/pharmacology
MH  - Hypertension/*physiopathology
MH  - Hypoxia/*physiopathology
MH  - Male
MH  - Nitroprusside/pharmacology
MH  - Potassium Channel Blockers
MH  - Rats
MH  - Rats, Inbred SHR
MH  - Rats, Inbred WKY
MH  - Scorpion Venoms/pharmacology
MH  - *Vasodilation/drug effects
EDAT- 1995/04/01 00:00
MHDA- 1995/04/01 00:01
CRDT- 1995/04/01 00:00
PHST- 1995/04/01 00:00 [pubmed]
PHST- 1995/04/01 00:01 [medline]
PHST- 1995/04/01 00:00 [entrez]
AID - 10.1161/01.hyp.25.4.735 [doi]
PST - ppublish
SO  - Hypertension. 1995 Apr;25(4 Pt 2):735-8. doi: 10.1161/01.hyp.25.4.735.