PMID- 15271663
OWN - NLM
STAT- MEDLINE
DCOM- 20050103
LR  - 20200930
IS  - 0363-6135 (Print)
IS  - 0363-6135 (Linking)
VI  - 287
IP  - 6
DP  - 2004 Dec
TI  - Biphasic modulation of vascular nitric oxide catabolism by oxygen.
PG  - H2421-6
AB  - Endothelium-derived nitric oxide (NO) plays an important role in the regulation 
      of vascular tone. Lack of NO bioavailability can result in cardiovascular 
      disease. NO bioavailability is determined by its rates of generation and 
      catabolism; however, it is not known how the NO catabolism rate is regulated in 
      the vascular wall under normoxic, hypoxic, and anaerobic conditions. To 
      investigate NO catabolism under different oxygen concentrations, studies of NO 
      and O2 consumption by the isolated rat aorta were performed using electrochemical 
      sensors. Under normoxic conditions, the rate of NO consumption in solution was 
      enhanced in the presence of the rat aorta. Under hypoxic conditions, NO 
      consumption decreased in parallel with the O2 concentration. Like the inhibition 
      of mitochondrial respiration by NO, the inhibitory effects of NO on aortic O2 
      consumption increased as O2 concentration decreased. Under anaerobic conditions, 
      however, a paradoxical reacceleration of NO consumption occurred. This increased 
      anaerobic NO consumption was inhibited by the cytochrome c oxidase inhibitor NaCN 
      but not by the free iron chelator deferoxamine, the flavoprotein inhibitor 
      diphenylene iodonium (10 microM), or superoxide dismutase (200 U/ml). The effect 
      of O2 on the NO consumption could be reproduced by purified cytochrome c oxidase 
      (CcO), implying that CcO is involved in aortic NO catabolism. This reduced NO 
      catabolism at low O2 tensions supports the maintenance of effective NO levels in 
      the vascular wall, reducing the resistance of blood vessels. The increased 
      anaerobic NO catabolism may be important for removing excess NO accumulation in 
      ischemic tissues.
FAU - Liu, Xiaoping
AU  - Liu X
AD  - Davis Heart and Lung Research Institute, The Ohio State Univ., 473 W. 12th Ave., 
      Columbus, OH 43210, USA. Liu-11@medctr.osu.edu
FAU - Cheng, Crystal
AU  - Cheng C
FAU - Zorko, Nicholas
AU  - Zorko N
FAU - Cronin, Scott
AU  - Cronin S
FAU - Chen, Yeong-Renn
AU  - Chen YR
FAU - Zweier, Jay L
AU  - Zweier JL
LA  - eng
GR  - K22 ES011031/ES/NIEHS NIH HHS/United States
GR  - HL-38324/HL/NHLBI NIH HHS/United States
GR  - HL-63744/HL/NHLBI NIH HHS/United States
GR  - HL65608/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
DEP - 20040722
PL  - United States
TA  - Am J Physiol Heart Circ Physiol
JT  - American journal of physiology. Heart and circulatory physiology
JID - 100901228
RN  - 31C4KY9ESH (Nitric Oxide)
RN  - EC 1.9.3.1 (Electron Transport Complex IV)
RN  - S88TT14065 (Oxygen)
SB  - IM
MH  - Animals
MH  - Aorta, Thoracic/*metabolism
MH  - Electron Transport Complex IV/metabolism
MH  - Hypoxia/*metabolism
MH  - In Vitro Techniques
MH  - Male
MH  - Nitric Oxide/*metabolism
MH  - Oxygen/*metabolism/pharmacology
MH  - Oxygen Consumption
MH  - Rats
MH  - Rats, Sprague-Dawley
EDAT- 2004/07/24 05:00
MHDA- 2005/01/04 09:00
CRDT- 2004/07/24 05:00
PHST- 2004/07/24 05:00 [pubmed]
PHST- 2005/01/04 09:00 [medline]
PHST- 2004/07/24 05:00 [entrez]
AID - 00487.2004 [pii]
AID - 10.1152/ajpheart.00487.2004 [doi]
PST - ppublish
SO  - Am J Physiol Heart Circ Physiol. 2004 Dec;287(6):H2421-6. doi: 
      10.1152/ajpheart.00487.2004. Epub 2004 Jul 22.