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Difference between revisions of "Hickey 2009 Am J Physiol Cell Physiol"

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(Created page with "{{Publication |title=Hickey AJ, Chai CC, Choong SY, de Freitas Costa S, Skea GL, Phillips AR, Cooper GJ (2009) Impaired ATP turnover and ADP supply depress cardiac mitochondrial ...")
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|authors=Hickey AJ, Chai CC, Choong SY, de Freitas Costa S, Skea GL, Phillips AR, Cooper GJ Β 
|authors=Hickey AJ, Chai CC, Choong SY, de Freitas Costa S, Skea GL, Phillips AR, Cooper GJ Β 
|year=2009
|year=2009
|abstract=Although most attention has been
|abstract=Although most attention has been focused on mitochondrial ATP production and transfer in failing
focused on mitochondrial ATP production and transfer in failing
hearts, less has been focused on the nonfailing hypertensive heart. Here, energetic complications are less obvious, yet they may provide
hearts, less has been focused on the nonfailing hypertensive heart.
insight into disease ontogeny. We studied hearts from 12-mo-old spontaneously hypertensive rats (SHR) relative to normotensive Wistar-Kyoto (WKY) rats. The ex vivo working-heart model of SHR showed reduced compliance and impaired responses to increasing preloads. High-resolution respirometry showed higher state 3 (with excess ADP) respiration in SHR left ventricle fibers with complex I substrates and maximal uncoupled respiration with complex I + complex II substrates. Respiration with ATP was depressed 15% in SHR fibers relative to WKY fibers, suggesting impaired ATP hydrolysis. This finding was consistent with a 50% depression of actomyosin ATPase activities. Superoxide production from SHR fibers was similar to that from WKY fibers respiring with ADP; however, it was increased by 15% with ATP. In addition, the apparent Km for ADP
Here, energetic complications are less obvious, yet they may provide
was 54% higher for SHR fibers, and assays conducted after ''ex vivo'' work showed a 28% depression of complex I in SHR, but not WKY, fibers. Transmission electron microscopy showed similar mitochondrial volumes but a decrease in the number of cristae in SHR mitochondria. Tissue lipid peroxidation was also 15% greater in SHR left ventricle. Overall, these data suggest that although cardiac mitochondria from nonfailing SHR hearts function marginally better than those from WKY hearts, they show dysfunction after intense work. Impaired ATP turnover in hard-working SHR hearts may starve cardiac mitochondria of ADP and elevate superoxide.
insight into disease ontogeny. We studied hearts from 12-mo-old
spontaneously hypertensive rats (SHR) relative to normotensive
Wistar-Kyoto (WKY) rats. The ex vivo working-heart model of SHR
showed reduced compliance and impaired responses to increasing
preloads. High-resolution respirometry showed higher state 3 (with
excess ADP) respiration in SHR left ventricle fibers with complex I
substrates and maximal uncoupled respiration with complex I οΏ½
complex II substrates. Respiration with ATP was depressed 15% in
SHR fibers relative to WKY fibers, suggesting impaired ATP hydrolysis.
This finding was consistent with a 50% depression of actomyosin
ATPase activities. Superoxide production from SHR fibers was
similar to that from WKY fibers respiring with ADP; however, it was
increased by 15% with ATP. In addition, the apparent Km for ADP
was 54% higher for SHR fibers, and assays conducted after ex vivo
work showed a 28% depression of complex I in SHR, but not WKY,
fibers. Transmission electron microscopy showed similar mitochondrial
volumes but a decrease in the number of cristae in SHR
mitochondria. Tissue lipid peroxidation was also 15% greater in SHR
left ventricle. Overall, these data suggest that although cardiac mitochondria
from nonfailing SHR hearts function marginally better than
those from WKY hearts, they show dysfunction after intense work.
Impaired ATP turnover in hard-working SHR hearts may starve
cardiac mitochondria of ADP and elevate superoxide.
|keywords=adenylate control, saponin-permeabilized fibers, hypertensive heart, oxidative stress, complex I dysfunction; respiration
|keywords=adenylate control, saponin-permeabilized fibers, hypertensive heart, oxidative stress, complex I dysfunction; respiration
|info=[http://www.ncbi.nlm.nih.gov/pubmed/19553568 PMID: 19553568]
|info=[http://www.ncbi.nlm.nih.gov/pubmed/19553568 PMID: 19553568]

Revision as of 14:53, 17 September 2010

Publications in the MiPMap
Hickey AJ, Chai CC, Choong SY, de Freitas Costa S, Skea GL, Phillips AR, Cooper GJ (2009) Impaired ATP turnover and ADP supply depress cardiac mitochondrial respiration and elevate superoxide in nonfailing spontaneously hypertensive rat hearts. Am J Physiol Cell Physiol 297: C766–C774.

Β» PMID: 19553568

Hickey AJ, Chai CC, Choong SY, de Freitas Costa S, Skea GL, Phillips AR, Cooper GJ (2009)

Abstract: Although most attention has been focused on mitochondrial ATP production and transfer in failing hearts, less has been focused on the nonfailing hypertensive heart. Here, energetic complications are less obvious, yet they may provide insight into disease ontogeny. We studied hearts from 12-mo-old spontaneously hypertensive rats (SHR) relative to normotensive Wistar-Kyoto (WKY) rats. The ex vivo working-heart model of SHR showed reduced compliance and impaired responses to increasing preloads. High-resolution respirometry showed higher state 3 (with excess ADP) respiration in SHR left ventricle fibers with complex I substrates and maximal uncoupled respiration with complex I + complex II substrates. Respiration with ATP was depressed 15% in SHR fibers relative to WKY fibers, suggesting impaired ATP hydrolysis. This finding was consistent with a 50% depression of actomyosin ATPase activities. Superoxide production from SHR fibers was similar to that from WKY fibers respiring with ADP; however, it was increased by 15% with ATP. In addition, the apparent Km for ADP was 54% higher for SHR fibers, and assays conducted after ex vivo work showed a 28% depression of complex I in SHR, but not WKY, fibers. Transmission electron microscopy showed similar mitochondrial volumes but a decrease in the number of cristae in SHR mitochondria. Tissue lipid peroxidation was also 15% greater in SHR left ventricle. Overall, these data suggest that although cardiac mitochondria from nonfailing SHR hearts function marginally better than those from WKY hearts, they show dysfunction after intense work. Impaired ATP turnover in hard-working SHR hearts may starve cardiac mitochondria of ADP and elevate superoxide. β€’ Keywords: adenylate control, saponin-permeabilized fibers, hypertensive heart, oxidative stress, complex I dysfunction; respiration


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Organism: Rat  Tissue;cell: Cardiac Muscle"Cardiac Muscle" is not in the list (Heart, Skeletal muscle, Nervous system, Liver, Kidney, Lung;gill, Islet cell;pancreas;thymus, Endothelial;epithelial;mesothelial cell, Blood cells, Fat, ...) of allowed values for the "Tissue and cell" property. 


Regulation: Respiration; OXPHOS; ETS Capacity"Respiration; OXPHOS; ETS Capacity" is not in the list (Aerobic glycolysis, ADP, ATP, ATP production, AMP, Calcium, Coupling efficiency;uncoupling, Cyt c, Flux control, Inhibitor, ...) of allowed values for the "Respiration and regulation" property. 


HRR: Oxygraph-2k