PMID- 21652603
OWN - NLM
STAT- MEDLINE
DCOM- 20110912
LR  - 20220408
IS  - 1535-3699 (Electronic)
IS  - 1535-3699 (Linking)
VI  - 236
IP  - 7
DP  - 2011 Jul
TI  - Intermittent hypoxia conditioning prevents endothelial dysfunction and improves 
      nitric oxide storage in spontaneously hypertensive rats.
PG  - 867-73
LID - 10.1258/ebm.2011.011023 [doi]
AB  - Although intermittent hypoxia is often associated with hypertension, experimental 
      and clinical studies have demonstrated definite antihypertensive effects of some 
      intermittent hypoxia conditioning (IHC) regimens. Mechanisms of this 
      antihypertensive response are unknown. Endothelial dysfunction related to 
      disturbed synthesis and/or reduced availability of nitric oxide (NO) has been 
      linked to hypertension. Thus, experiments were conducted to determine if IHC can 
      improve endothelium-dependent relaxation and formation of releasable vascular NO 
      stores of young (4-8-week-old) spontaneously hypertensive rats (SHR). Rats were 
      subjected to either IHC (9.5-10% O(2), 5-10 min, 5-8 times per day, 20 d) or to 
      sham conditioning. Endothelium-dependent relaxation to acetylcholine was measured 
      in norepinephrine-precontracted, isolated aortic rings, and the size of NO stores 
      was evaluated by percent relaxation to N-acetylcysteine (NAC), which releases 
      stored NO. The capacity of aortic rings for NO storage was evaluated by the 
      relaxation to NAC after prior incubation with an NO donor. IHC significantly 
      suppressed the development of hypertension in young SHR. Endothelial function 
      decreased from 54.7 +/- 4.6% to 28.1 +/- 6.4% relaxation to acetylcholine after 20 d 
      of sham IHC, whereas endothelial function was sustained (60.3 +/- 6.0% relaxation) 
      in IHC rats. IHC also induced formation of available NO stores and enhanced the 
      capacity of aortic rings to store NO. Therefore, the antihypertensive effect of 
      IHC in young SHR is associated with prevention of endothelial dysfunction and 
      with increased accumulation of NO stores in vascular walls.
FAU - Manukhina, Eugenia B
AU  - Manukhina EB
AD  - Department of Integrative Physiology, University of North Texas Health Science 
      Center, 3500 Camp Bowie Blvd, Fort Worth, TX 76107, USA.
FAU - Jasti, Dinesh
AU  - Jasti D
FAU - Vanin, Anatoly F
AU  - Vanin AF
FAU - Downey, H Fred
AU  - Downey HF
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20110607
PL  - Switzerland
TA  - Exp Biol Med (Maywood)
JT  - Experimental biology and medicine (Maywood, N.J.)
JID - 100973463
RN  - 0 (Vasodilator Agents)
RN  - 31C4KY9ESH (Nitric Oxide)
RN  - N9YNS0M02X (Acetylcholine)
SB  - IM
MH  - Acetylcholine/pharmacology
MH  - Animals
MH  - Aorta/drug effects
MH  - *Conditioning, Psychological
MH  - Endothelial Cells/*drug effects/*metabolism
MH  - Hypertension/prevention & control
MH  - *Hypoxia
MH  - Muscle, Smooth, Vascular/drug effects
MH  - Nitric Oxide/*metabolism
MH  - Rats
MH  - Rats, Inbred SHR
MH  - Vasodilator Agents/pharmacology
EDAT- 2011/06/10 06:00
MHDA- 2011/09/13 06:00
CRDT- 2011/06/10 06:00
PHST- 2011/06/10 06:00 [entrez]
PHST- 2011/06/10 06:00 [pubmed]
PHST- 2011/09/13 06:00 [medline]
AID - ebm.2011.011023 [pii]
AID - 10.1258/ebm.2011.011023 [doi]
PST - ppublish
SO  - Exp Biol Med (Maywood). 2011 Jul;236(7):867-73. doi: 10.1258/ebm.2011.011023. 
      Epub 2011 Jun 7.