PMID- 27233303
OWN - NLM
STAT- MEDLINE
DCOM- 20161013
LR  - 20210109
IS  - 2051-817X (Electronic)
IS  - 2051-817X (Linking)
VI  - 4
IP  - 10
DP  - 2016 May
TI  - Aging does not affect soluble guanylate cyclase redox state in mouse aortas.
LID - 10.14814/phy2.12816 [doi]
LID - e12816
AB  - Aging is associated with endothelial dysfunction, defined as a reduction in 
      nitric oxide (NO) bioavailability. Although the redox state of the NO acceptor 
      soluble guanylate cyclase (sGC) is another determinant factor for its 
      bioavailability and is disturbed by reactive oxygen species (ROS) known to be 
      increased with age, it is unclear whether aging actually has an impact on 
      vascular sGC redox equilibrium. Therefore, this study investigated this issue 
      using two different types of compounds, the sGC stimulator BAY 41-2272 and the 
      sGC activator BAY 60-2770. Plasma thiobarbituric acid-reactive substances (TBARS) 
      levels were markedly higher in aged (19-20 months old) mice than in young 
      (2-3 months old) mice, whereas superoxide levels in endothelium-denuded aortas 
      were not different between the groups. The relaxant response of 
      endothelium-denuded aortas to either BAY 41-2272 or BAY 60-2770 was identical in 
      aged and young mice. In addition, the vascular cGMP production stimulated with 
      BAY 41-2272 or BAY 60-2770 in aged mice was the same level as that in young mice. 
      These findings suggest that aging accompanied by an increase in systemic 
      oxidative stress does not affect vascular smooth muscle ROS generation and sGC 
      redox equilibrium. Unless ROS are increased in vascular smooth muscle, the sGC 
      redox equilibrium might remain unchanged.
CI  - (c) 2016 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on 
      behalf of the American Physiological Society and The Physiological Society.
FAU - Shimosato, Takashi
AU  - Shimosato T
AD  - Department of Pharmacology, Shiga University of Medical Science, Otsu, Shiga, 
      Japan.
FAU - Tawa, Masashi
AU  - Tawa M
AD  - Department of Pharmacology, Shiga University of Medical Science, Otsu, Shiga, 
      Japan tawa@belle.shiga-med.ac.jp.
FAU - Iwasaki, Hirotaka
AU  - Iwasaki H
AD  - Department of Pharmacology, Shiga University of Medical Science, Otsu, Shiga, 
      Japan.
FAU - Imamura, Takeshi
AU  - Imamura T
AD  - Department of Pharmacology, Shiga University of Medical Science, Otsu, Shiga, 
      Japan.
FAU - Okamura, Tomio
AU  - Okamura T
AD  - Department of Pharmacology, Shiga University of Medical Science, Otsu, Shiga, 
      Japan.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Physiol Rep
JT  - Physiological reports
JID - 101607800
RN  - 0 
      (3-(4-Amino-5-cyclopropylpyrimidine-2-yl)-1-(2-fluorobenzyl)-1H-pyrazolo(3,4-b)pyridine)
RN  - 0 (4-(((4-carboxybutyl) (2- (5-fluoro-2-((4'-(trifluoromethyl) 
      biphenyl-4-yl)methoxy)phenyl)ethyl) amino)methyl)benzoic acid)
RN  - 0 (Benzoates)
RN  - 0 (Biphenyl Compounds)
RN  - 0 (Hydrocarbons, Fluorinated)
RN  - 0 (Pyrazoles)
RN  - 0 (Pyridines)
RN  - 0 (Receptors, Cytoplasmic and Nuclear)
RN  - EC 4.6.1.2 (Guanylate Cyclase)
RN  - EC 4.6.1.2 (Soluble Guanylyl Cyclase)
SB  - IM
MH  - Aging/drug effects/*metabolism
MH  - Animals
MH  - Aorta, Thoracic/drug effects/*metabolism
MH  - Benzoates/pharmacology
MH  - Biphenyl Compounds/pharmacology
MH  - Guanylate Cyclase/*metabolism
MH  - Hydrocarbons, Fluorinated/pharmacology
MH  - Male
MH  - Mice
MH  - Organ Culture Techniques
MH  - Oxidation-Reduction/drug effects
MH  - Pyrazoles/pharmacology
MH  - Pyridines/pharmacology
MH  - Receptors, Cytoplasmic and Nuclear/*metabolism
MH  - Soluble Guanylyl Cyclase
PMC - PMC4886176
OTO - NOTNLM
OT  - Aging
OT  - nitric oxide
OT  - sGC activator
OT  - sGC stimulator
OT  - soluble guanylate cyclase
EDAT- 2016/05/29 06:00
MHDA- 2016/05/29 06:01
PMCR- 2016/05/27
CRDT- 2016/05/29 06:00
PHST- 2016/05/04 00:00 [received]
PHST- 2016/05/07 00:00 [accepted]
PHST- 2016/05/29 06:00 [entrez]
PHST- 2016/05/29 06:00 [pubmed]
PHST- 2016/05/29 06:01 [medline]
PHST- 2016/05/27 00:00 [pmc-release]
AID - 4/10/e12816 [pii]
AID - PHY212816 [pii]
AID - 10.14814/phy2.12816 [doi]
PST - ppublish
SO  - Physiol Rep. 2016 May;4(10):e12816. doi: 10.14814/phy2.12816.