| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
1 Department of Physiology and Biophysics, College of Medicine, Inje University, Busan, Korea, Republic of
2 Department of Pharmaceutical Engineering, Silla University, Busan, Korea, Republic of
* To whom correspondence should be addressed. E-mail: phyhanj{at}ijnc.inje.ac.kr.
Nitric oxide (NO) plays an important role in anoxic preconditioning to protect the heart against ischemia/reperfusion (I/R) injuries. The present work was performed to study better the NO-cGMP-PKG signaling pathway in the activation of both sarcolemmal and mitochondrial ATP-sensitive K+ (KATP) channels during anoxic preconditioning (APC) and final influence on reducing anoxia/reperfusion (A/R)-induced cardiac damage in rat hearts. The upstream regulating elements controlling NO-cGMP-PKG signal-induced KATP channel opening that leads to cardioprotection were investigated. The involvement of both inducible and endothelial NO synthases (iNOS, eNOS) in the progression of this signaling pathway was followed. Final cellular outcomes of ischemia-induced injury after different preconditioning in the form of LDH release, DNA strand breaks and MDA formation in rat hearts as indices of cell injury and lipid peroxidation, respectively, were investigated. The LDH and MDA values decreased in the groups that underwent three, 5-min preconditioning periods with pinacidil (50 µM), diazoxide (100 µM), S-nitroso-N-acetylpenicillamine (SNAP, 300 µM), or phenyl-1,N2-etheno-8-bromo guanosine-3',5'-cyclic monophosphorothioate, Sp-isomer (Sp-8-Br-PET-cGMPS, 10 µM) prior to the A/R period. Preconditioning with SNAP significantly reduced the DNA damage. The effect was blocked by the presence of glibenclamide (50 µM), 5-hydroxydecanoate (5-HD, 100 µM), N(G)-nitro-L-arginine methyl ester (L-NAME, 200 µM), and phenyl-1,N2-etheno-8-bromoguanosine-3',5'-cyclic monophosphorothioate, Rp-isomer (Rp-8-Br-PET-cGMPS, 1 µM). The results suggest iNOS, rather than eNOS, as major contributing NO synthase during APC treatment. Moreover, the PKG shows priority over NO as upstream regulator of NO-cGMP-PKG signal-induced KATP channel opening that leads to cardioprotection during APC treatment.
This article has been cited by other articles:
|
|
 |
|
  G. A. B. Armstrong, C. I. Rodgers, T. G. A. Money, and R. M. Robertson Suppression of Spreading Depression-Like Events in Locusts by Inhibition of the NO/cGMP/PKG Pathway J. Neurosci., June 24, 2009; 29(25): 8225 - 8235. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C.-S. Kang, C.-C. Chen, C.-C. Lin, N.-C. Chang, and T.-M. Lee Effect of ATP-sensitive potassium channel agonists on sympathetic hyperinnervation in postinfarcted rat hearts Am J Physiol Heart Circ Physiol, June 1, 2009; 296(6): H1949 - H1959. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. J. Franco, D. C. Fernandez, P. H. Sande, M. I. Keller Sarmiento, M. Chianelli, D. A. Saenz, and R. E. Rosenstein Effect of Bacterial Lipopolysaccharide on Ischemic Damage in the Rat Retina Invest. Ophthalmol. Vis. Sci., October 1, 2008; 49(10): 4604 - 4612. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Miyamae, S. Sugioka, and V. M. Figueredo Additive Cardioprotection by Ethanol and Sevoflurane: Are Sarcolemmal KATP Channels Also Involved? Anesth. Analg., June 1, 2008; 106(6): 1926 - 1927. [Full Text] [PDF]
|
|
|
|
 |
|
 M. Orio, A. Kunz, T. Kawano, J. Anrather, P. Zhou, and C. Iadecola Lipopolysaccharide Induces Early Tolerance to Excitotoxicity via Nitric Oxide and cGMP Stroke, October 1, 2007; 38(10): 2812 - 2817. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. V. Cuong, M. Warda, N. Kim, W. S. Park, J. H. Ko, E. Kim, and J. Han Dynamic changes in nitric oxide and mitochondrial oxidative stress with site-dependent differential tissue response during anoxic preconditioning in rat heart Am J Physiol Heart Circ Physiol, September 1, 2007; 293(3): H1457 - H1465. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. Penna, D. Mancardi, R. Rastaldo, G. Losano, and P. Pagliaro Intermittent activation of bradykinin B2 receptors and mitochondrial KATP channels trigger cardiac postconditioning through redox signaling Cardiovasc Res, July 1, 2007; 75(1): 168 - 177. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Y. Wang, N. Ahmad, B. Wang, and M. Ashraf Chronic preconditioning: a novel approach for cardiac protection Am J Physiol Heart Circ Physiol, May 1, 2007; 292(5): H2300 - H2305. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. K. Arrell, S. T. Elliott, L. A. Kane, Y. Guo, Y. H. Ko, P. L. Pedersen, J. Robinson, M. Murata, A. M. Murphy, E. Marban, et al. Proteomic Analysis of Pharmacological Preconditioning: Novel Protein Targets Converge to Mitochondrial Metabolism Pathways Circ. Res., September 29, 2006; 99(7): 706 - 714. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Visit Other APS Journals Online |
