Mitochondrial contribution to the molecular mechanism of heart acclimatization to chronic hypoxia: role of nitric oxide.
A remarkable number of adaptive responses; including changes in the cardiovascular, respiratory and hematologic systems; takes place during acclimatization to natural or simulated high altitude. This adaptation to chronic hypoxia confers the heart an improved tolerance to all major deleterious consequences of acute O2 deprivation, not only reducing infarct size but also alleviating post-ischemic contractile dysfunction and ventricular arrhythmias. There is growing evidence about the involvement of mitochondria and NO in the establishment of cardioprotection. This review focuses on evidence about the putative role of different effectors of heart acclimatization to chronic hypoxia. Along with classical parameters, we consider NO, specially that generated by mtNOS, mitochondrial respiratory chain, mitoK(ATP) channels, reactive oxygen species and control of gene expression by HIF-1.
Zaobornyj
Tamara
T
Laboratory of Free Radical Biology, School of Pharmacy and Biochemistry, University of Buenos Aires, C1113AAD, Buenos Aires, Argentina. tamaraz@ffyb.uba.ar
Gonzales
Gustavo F
GF
Valdez
Laura B
LB
D000064:Acclimatization; D000818:Animals; D006801:Humans; D000860:Hypoxia / Q000378:metabolism*; D051793:Hypoxia-Inducible Factor 1 / Q000502:physiology; D051379:Mice; D008929:Mitochondria, Heart / Q000378:metabolism*; D009569:Nitric Oxide / Q000502:physiology*; D015221:Potassium Channels / Q000502:physiology; D051381:Rats
D051793:Hypoxia-Inducible Factor 1; D015221:Potassium Channels; D009569:Nitric Oxide