Expression of mitochondrial regulatory genes parallels respiratory capacity and contractile function in a rat model of hypoxia-induced right ventricular hypertrophy

Chronic hypobaric hypoxia (CHH) increases load on the right ventricle (RV) resulting in RV hypertrophy. We hypothesized that CHH elicits distinct responses, i.e., the hypertrophied RV, unlike the left ventricle (LV), displaying enhanced mitochondrial respiratory and contractile function. Wistar rats...

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Bibliographic Details
Published in:Molecular and Cellular Biochemistry
Main Authors: Zungu M., Young M.E., Stanley W.C., Essop M.F.
Format: Article in Journal/Newspaper
Language:unknown
Published: 2008
Subjects:
animal cell
animal experiment
animal model
article
controlled study
gene expression
heart contraction
heart function
heart left ventricle
heart right ventricle
heart right ventricle hypertrophy
heart weight
hypoxia
male
mitochondrial respiration
mitochondrion
nonhuman
oxygen consumption
rat
regulator gene
respiration control
systolic blood pressure
upregulation
Wistar rat
Animals
Anoxia
Cell Respiration
Disease Models
Animal
Gene Expression Regulation
Genes
Regulator
Heart Function Tests
Hemodynamics
Hypertrophy
Right Ventricular
Mitochondria
Myocardial Contraction
Rats
Wistar
RNA
Messenger
Rattus
Rattus norvegicus
Rattus rattus
Online Access:http://hdl.handle.net/10019.1/11476
https://doi.org/10.1007/s11010-008-9867-5
Description
Summary:Chronic hypobaric hypoxia (CHH) increases load on the right ventricle (RV) resulting in RV hypertrophy. We hypothesized that CHH elicits distinct responses, i.e., the hypertrophied RV, unlike the left ventricle (LV), displaying enhanced mitochondrial respiratory and contractile function. Wistar rats were exposed to 4 weeks CHH (11% O2) versus normoxic controls. RV/body weight ratio increased (P < 0.001 vs. control) while RV systolic and developed pressures were higher. However, LV systolic and developed pressures were significantly reduced. Mitochondrial O2 consumption was sustained in the hypertrophied RV, ADP/O increased (P < 0.01 vs. control) and proton leak significantly decreased. Conversely, LV mitochondrial O2 consumption was attenuated (P < 0.05 vs. control) and proton leak significantly increased. In parallel, expression of mitochondrial regulators was upregulated in the hypertrophied RV but not the LV. Our data show that the hypertrophied RV induces expression of mitochondrial regulatory genes linking respiratory capacity and enhanced efficiency to sustained contractile function. © Springer Science+Business Media, LLC. 2008. Article

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