Prolonged oxidative stress inverts the cardiac force–frequency relation: role of altered calcium handling and myofilament calcium responsiveness

2006 ◽  
Vol 40 (1) ◽  
pp. 64-75 ◽  
Author(s):  
Jianzhu Luo ◽  
Yu-Ting Xuan ◽  
Yan Gu ◽  
Sumanth D. Prabhu
2010 ◽  
Vol 98 (3) ◽  
pp. 356a
Author(s):  
Genaro A. Ramirez-Correa ◽  
Sonia Cortassa ◽  
Brian Stanley ◽  
Wei Dong Gao ◽  
Anne M. Murphy

2004 ◽  
Vol 22 (Suppl. 2) ◽  
pp. S187
Author(s):  
J. Loukotová ◽  
J. Tichá ◽  
J. Kunes ◽  
J. Zicha

Circulation ◽  
1995 ◽  
Vol 92 (5) ◽  
pp. 1169-1178 ◽  
Author(s):  
Burkert Pieske ◽  
Bodo Kretschmann ◽  
Markus Meyer ◽  
Christian Holubarsch ◽  
Jörg Weirich ◽  
...  

Nutrients ◽  
2019 ◽  
Vol 11 (9) ◽  
pp. 2090 ◽  
Author(s):  
Thomas Senoner ◽  
Wolfgang Dichtl

Cardiovascular diseases (CVD) are complex entities with heterogenous pathophysiologic mechanisms and increased oxidative stress has been viewed as one of the potential common etiologies. A fine balance between the presence of reactive oxygen species (ROS) and antioxidants is essential for the proper normal functioning of the cell. A basal concentration of ROS is indispensable for the manifestation of cellular functions, whereas excessive levels of ROS cause damage to cellular macromolecules such as DNA, lipids and proteins, eventually leading to necrosis and apoptotic cell death. CVD is the main cause of death worldwide with several conditions being affected by oxidative stress. Increased ROS lead to decreased nitric oxide availability and vasoconstriction, promoting arterial hypertension. ROS also negatively influence myocardial calcium handling, causing arrhythmia, and augment cardiac remodeling by inducing hypertrophic signaling and apoptosis. Finally, ROS have also been shown to promote atherosclerotic plaque formation. This review aims at giving an introduction into oxidative stress in CVD, with special focus on endothelial dysfunction, and then examining in detail the role of oxidative stress in the most prevalent of these diseases. Finally, potential nutraceuticals and diets that might be beneficial in diminishing the burden of oxidative stress in CVD are presented.


2007 ◽  
Vol 107 (6) ◽  
pp. 954-962 ◽  
Author(s):  
Paul M. Heerdt ◽  
Paul Lane ◽  
Brian Y. Pan ◽  
Ulrich Schaefer ◽  
Mark Crabtree ◽  
...  

Background Chronic, disease-associated oxidative stress induces myocardial peroxynitrite formation that may lead to nitrosative inhibition of the calcium cycling protein sarcoplasmic endoreticular calcium adenosine triphosphatase subtype 2a (SERCA2a). The current study was designed to test the hypothesis that the acute oxidative stress associated with lung resection also induces myocardial nitrosative stress and alters SERCA2a activity. Methods Ventricular myocardium from 16 swine was studied; 11 animals had undergone left upper lobectomy (n = 7) or sham thoracotomy (n = 4) 3 days before harvest, and 5 were nonoperated controls. Tissue peroxynitrite was assessed by measurement of 3-nitrotyrosine incorporation into proteins. SERCA2a activity was determined from indo-1 uptake by isolated sarcoplasmic reticular membranes. Expression of SERCA2a and its regulatory protein phospholamban were determined by Western blotting, as was the phospholamban phosphorylation state (when dephosporylated, phospholamban inhibits SERCA2a). Mechanical significance of changes in SERCA2a activity was assessed from the force-frequency relation of isometric myocardial trabeculae. Results Relative to both the control and sham groups, lobectomy animals exhibited a greater than twofold higher myocardial 3-nitrotyrosine incorporation and an approximately 50% lower SERCA2a activity, but no difference in SERCA2a or phospholamban expression or phospholamban phosphorylation. Concomitantly, whereas the trabecular force-frequency relation of control animals was positive, that of lobectomy animals was negative, consistent with impaired calcium cycling. Conclusions These data indicate that oxidative/nitrosative stress associated with lung resection influences SERCA2a activity independent of any influence on protein expression or phospholamban phosphorylation. The findings link an acute event with a subcellular process primarily described for chronic illness and suggest a biochemical basis for perioperative changes in myocardial mechanical reserve.


2015 ◽  
Vol 28 (5) ◽  
pp. 833-841 ◽  
Author(s):  
Camila B. Tromm ◽  
Bruna G. Pozzi ◽  
Carla S. Paganini ◽  
Scherolin O. Marques ◽  
Giulia S. Pedroso ◽  
...  

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