Document Detail


Erythrocyte-dependent regulation of human skeletal muscle blood flow: role of varied oxyhemoglobin and exercise on nitrite, S-nitrosohemoglobin, and ATP.
MedLine Citation:
PMID:  20852046     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The erythrocyte is proposed to play a key role in the control of local tissue perfusion via three O(2)-dependent signaling mechanisms: 1) reduction of circulating nitrite to vasoactive NO, 2) S-nitrosohemoglobin (SNO-Hb)-dependent vasodilatation, and 3) release of the vasodilator and sympatholytic ATP; however, their relative roles in vivo remain unclear. Here we evaluated each mechanism to gain insight into their roles in the regulation of human skeletal muscle blood flow during hypoxia and hyperoxia at rest and during exercise. Arterial and femoral venous hemoglobin O(2) saturation (O(2)Hb), plasma and erythrocyte NO and ATP metabolites, and leg and systemic hemodynamics were measured in 10 healthy males exposed to graded hypoxia, normoxia, and graded hyperoxia both at rest and during submaximal one-legged knee-extensor exercise. At rest, leg blood flow and NO and ATP metabolites in plasma and erythrocytes remained unchanged despite large alterations in O(2)Hb. During exercise, however, leg and systemic perfusion and vascular conductance increased in direct proportion to decreases in arterial and venous O(2)Hb (r(2) = 0.86-0.98; P = 0.01), decreases in venous plasma nitrite (r(2) = 0.93; P < 0.01), increases in venous erythrocyte nitroso species (r(2) = 0.74; P < 0.05), and to a lesser extent increases in erythrocyte SNO (r(2) = 0.59; P = 0.07). No relationship was observed with plasma ATP (r(2) = 0.01; P = 0.99) or its degradation compounds. These in vivo data indicate that, during low-intensity exercise and hypoxic stress, but not hypoxic stress alone, plasma nitrite consumption and formation of erythrocyte nitroso species are associated with limb vasodilatation and increased blood flow in the human skeletal muscle vasculature.
Authors:
Stéphane P Dufour; Rakesh P Patel; Angela Brandon; Xinjun Teng; James Pearson; Horace Barker; Leena Ali; Ada H Y Yuen; Ryszard T Smolenski; José González-Alonso
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2010-09-17
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  299     ISSN:  1522-1539     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2010 Dec 
Date Detail:
Created Date:  2010-12-03     Completed Date:  2011-01-13     Revised Date:  2013-05-27    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H1936-46     Citation Subset:  IM    
Affiliation:
Centre for Sports Medicine and Human Performance, Brunel University West London, Uxbridge, United Kingdom. sdufour@unistra.fr
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MeSH Terms
Descriptor/Qualifier:
Adenosine Triphosphate / blood*
Adult
Anoxia / blood,  physiopathology
Erythrocytes / metabolism*
Exercise*
Hemoglobins / metabolism*
Humans
Hyperoxia / blood,  physiopathology
Leg
Male
Muscle Contraction*
Muscle, Skeletal / blood supply*,  metabolism*
Nitric Oxide / blood
Nitrites / blood*
Oxygen / blood
Oxyhemoglobins / metabolism*
Regional Blood Flow
Time Factors
Vasodilation
Young Adult
Grant Support
ID/Acronym/Agency:
HL092624/HL/NHLBI NIH HHS; R01 HL092624/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Hemoglobins; 0/Nitrites; 0/Oxyhemoglobins; 0/S-nitrosohemoglobin; 10102-43-9/Nitric Oxide; 56-65-5/Adenosine Triphosphate; 7782-44-7/Oxygen
Comments/Corrections

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