| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
1 Medicine, Medical University of Ohio, Toledo, Ohio, United States
2 Medicine, Friendship Hospital, Beijing, China
3 Chinese Academy of Medical Sciences, The Institute of Nutrition and Food Hygiene, Beijing, China
4 Proteomics Core Laboratory, Medical University of Ohio, Toledo, Ohio, United States
* To whom correspondence should be addressed. E-mail: jshapiro{at}meduohio.edu.
The effect of cardiac glycosides to increase cardiac inotropy by altering Ca2+ cycling is well known but still poorly understood. The studies described in this report focus on defining the effects of ouabain signaling on sarcoplasmic reticulum Ca2+ ATPase function. Rat cardiac myocytes treated with 50 µM ouabain demonstrated substantial increases in systolic and diastolic Ca2+ concentrations. The recovery time constant for the Ca2+ transient, TauCa2+, was significantly prolonged by ouabain. Exposure to 10 µM H2O2, which causes a similar increase in intracellular reactive oxygen species as 50 µM ouabain, caused a similar increase in TauCa2+. Concurrent exposure to 10 mM N-Acetyl Cysteine or an aqueous extract from green tea (50 mg/ml) both prevented the increases in TauCa2+ as well as the changes in systolic or diastolic Ca2+ concentrations. We also observed that 50 µM ouabain induced increases in developed pressure in addition to diastolic dysfunction in the isolated perfused rat heart. Co-administration of ouabain with N-Acetyl Cysteine prevented these increases. Analysis of sarcoplasmic reticulum Ca2+ ATPase protein revealed increases in both the oxidation and nitrotyrosine content in the ouabain treated hearts. Liquid chromatography/mass spectrometric analysis confirmed that the sarcoplasmic reticulum Ca2+ ATPase protein from ouabain treated hearts had modifications consistent with oxidative and nitrosative stress. These data suggest that ouabain induces oxidative changes of the sarcoplasmic reticulumCa2+ ATPase structure and function which may, in turn, produce some of the associated changes in Ca2+ cycling and physiological function.
This article has been cited by other articles:
|
|
 |
|
  N. Morita, A. A. Sovari, Y. Xie, M. C. Fishbein, W. J. Mandel, A. Garfinkel, S.-F. Lin, P.-S. Chen, L.-H. Xie, F. Chen, et al. Increased susceptibility of aged hearts to ventricular fibrillation during oxidative stress Am J Physiol Heart Circ Physiol, November 1, 2009; 297(5): H1594 - H1605. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. Singh, M. Salih, and B. S. Tuana {alpha}-Kinase Anchoring Protein {alpha}KAP Interacts with SERCA2A to Spatially Position Ca2+/Calmodulin-dependent Protein Kinase II and Modulate Phospholamban Phosphorylation J. Biol. Chem., October 9, 2009; 284(41): 28212 - 28221. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. Y. Bagrov, J. I. Shapiro, and O. V. Fedorova Endogenous Cardiotonic Steroids: Physiology, Pharmacology, and Novel Therapeutic Targets Pharmacol. Rev., March 1, 2009; 61(1): 9 - 38. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 W. Schoner and G. Scheiner-Bobis Role of endogenous cardiotonic steroids in sodium homeostasis Nephrol. Dial. Transplant., September 1, 2008; 23(9): 2723 - 2729. [Full Text] [PDF]
|
|
|
|
|
|
D. Li, C. Yang, Y. Chen, J. Tian, L. Liu, Q. Dai, X. Wan, and Z. Xie Identification of a PKC{varepsilon}-dependent regulation of myocardial contraction by epicatechin-3-gallate Am J Physiol Heart Circ Physiol, January 1, 2008; 294(1): H345 - H353. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. Pasdois, C. L. Quinlan, A. Rissa, L. Tariosse, B. Vinassa, A. D. T. Costa, S. V. Pierre, P. Dos Santos, and K. D. Garlid Ouabain protects rat hearts against ischemia-reperfusion injury via pathway involving src kinase, mitoKATP, and ROS Am J Physiol Heart Circ Physiol, March 1, 2007; 292(3): H1470 - H1478. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Visit Other APS Journals Online |
