Contribution of the Na+ channel and Na+/H+ exchanger to the anoxic rise of [Na+] in ventricular myocytes

American Journal of Physiology - Heart and Circulatory Physiology

Volumn 277, Issue 5 46-5, 1999, Pages

  Eigel, B N ^a   Hadley, R W ^a  

^a UNIVERSITY OF KENTUCKY   (United States)

Author keywords

Heart; Ischemia; Sodium; Sodium binding benzofuran isophthalate

Indexed keywords

PROTON; SODIUM CHANNEL; SODIUM ION;

ANIMAL CELL; ANOXIA; ARTICLE; GUINEA PIG; HEART MUSCLE CELL; HEART MUSCLE ISCHEMIA; HEART PROTECTION; HEART VENTRICLE WALL; HYPERKALEMIA; NONHUMAN; PRIORITY JOURNAL; PROTON SODIUM EXCHANGE; SODIUM TRANSPORT;

EID: 0032712620     PISSN: 03636135     EISSN: None     Source Type: Journal    
DOI: 10.1152/ajpheart.1999.277.5.h1817     Document Type: Article

References (34)

1. 2+ in single rat heart cells during anoxia and reoxygenation. Biochem. J. 244: 381-385, 1987.
2. Anderson, S. E., E. Murphy, C. Steenbergen, R. E. London, and P. M. Gala. Na-H exchange in myocardium: effects of hypoxia and acidification on Na and Ca. Am. J. Physiol. 259 (Cell Physiol. 28): C940-C948, 1990.
3. Donoso, P., J. G. Mill, S. C. O'Neill, and D. A. Eisner. Fluorescence measurements of cytoplasmic and mitochondrial sodium concentrations in rat ventricular myocytes. J. Physiol. (Lond.) 448: 493-509, 1992.
4. + entry, J. Mol. Cell. Cardiol. 30: 829-835, 1998.
5. Hadley, R. W., and W. J. Lederer. Ca and voltage inactivate Ca channels in guinea pig ventricular myocytes through independent mechanisms. J. Physiol. (Lond.) 444: 257-268, 1991.
6. 2+ exchange. Circ. Res. 71: 547-557, 1992.
7. Haigney, M. C. P., E. G. Lakatta, M. D. Stern, and H. S. Silverman. Sodium channel blockade reduces hypoxic sodium loading and sodium-dependent calcium loading. Circulation 90: 391-399, 1994.
8. Hotta, Y., M. Fujita, J. Nakagawa, H. Ando, K. Takeya, N. Ishikawa, and J. Sakakibara. Contribution of cytosolic ionic and energetic milieu change to ischemia-and reperfusion-induced injury in guinea pig heart: fluorometry and nuclear magnetic resonance studies. J. Cardiovasc. Electrophysiol. 31: 146-156, 1998.
9. + exchange against stunning. J. Mol. Cell. Cardiol. 30: 509-517, 1998.
10. Ju, Y., D. A. Saint, and P. W. Gage. Hypoxia increases persistent sodium current in rat ventricular myocytes. J. Physiol. (Lond.) 497: 337-347, 1996.
11. Li, Q. A., R. A. Altschuld, and B. T. Stokes. Myocyte deenergization and intracellular free calcium dynamics. Am. J. Physiol. 255 (Cell Physiol. 24): C162-C168, 1988.
12. Liu, H., P. M. Cala, and S. E. Anderson. Ethylisopropylamiloride diminishes changes in intracellular Na, Ca and pH in ischemic newborn myocardium. J. Mol. Cell. Cardiol. 29: 2077-2086, 1997.
13. Mejia-Alvarez, R., and E. Marban. Mechanism of the increase in intracellular sodium during metabolic inhibition, direct evidence against mediation by voltage-dependent sodium channels. J. Mol. Cell. Cardiol. 24: 1307-1320, 1992.
14. Murphy, E., M. Perlman, R. E. London, and C. Steenbergen. Amiloride delays the ischemia-induced rise in cytosolic free calcium. Circ. Res. 68: 1250-1258, 1991.
15. Murphy, J. G., T. W. Smith, and J. D. Marsh. Mechanisms of reoxygenation-induced calcium overload in cultured chick embryo heart cells. Am. J. Physiol. 254 (Heart Circ. Physiol. 23): H1133-H1141, 1988.
16. Narahashi, T., J. W. Moore, and W. R. Scott. Tetrodotoxin blockage of sodium conductance increase in lobster giant axons. J. Gen. Physiol. 47: 965-974, 1964.
17. Orlowski, J., R. A. Kandasamy, and G. E. Shull. Molecular cloning of putative members of the Na/H exchanger gene family. J. Biol. Chem. 267: 9331-9339, 1992.
18. Pierce, G. N., and M. P. Czubryt. The contribution of ionic imbalance to ischemia/reperfusion-induced injury. J. Mol. Cell. Cardiol. 27: 53-63, 1995.
19. + exchange. Am. J. Physiol. 265 (Heart Circ. Physiol. 34): H2017-H2026, 1993.
20. Piper, H. M., B. Siegmund, Y. V. Ladilov, and K. Schluter. Calcium and sodium control in hypoxic-reoxygenated cardiomyocytes. Basic Res. Cardiol. 88: 471-482, 1993.
21. +], and pH in guinea pig ventricular myocytes exposed to anoxia and reoxygenation. Am. J. Physiol. 272 (Heart Circ. Physiol. 41): H2679-H2685, 1997.
22. + -exchange inhibitor HOE-642 on intracellular pH, calcium and sodium in isolated rat ventricular myocytes. Pflügers Arch. 433: 26-34, 1996.
23. 2+]i during metabolic inhibition. Am. J. Physiol. 268 (Heart Circ. Physiol. 37): H1239-H1248, 1995.
24. Scholz, W., and U. Albus. Potential of selective sodium-hydrogen exchange inhibitors in cardiovascular therapy. Cardiovasc. Res. 29: 184-188 1995.
25. Scholz, W., U. Albus, L. Counillon, H. Gögelein, H. J. Lang, W. Linz, A. Weichert, and B. A. Scholkens. Protective effects of HOE642, a selective sodium-hydrogen exchange subtype 1 inhibitor, on cardiac ischaemia and reperfusion. Cardiovasc. Res. 29: 260-268, 1995.
26. Scholz, W., U. Albus, H. J. Lang, W. Linz, P. A. Martorana, H. C. Englert, and B. A. Schölkens. Hoe 694, a new Na/H exchange inhibitor and its effects in cardiac ischemia. Br. J. Pharmacol. 109: 562-568, 1993.
27. Shander, G. S., A. I. Undrovinas, and J. C. Makielski. Rapid onset of lysophosphatidylcholine-induced modification of whole cell cardiac sodium kinetics. J. Mol. Cell. Cardiol. 28: 743-753, 1996.
28. 2+ overload. Am. J. Physiol. 263 (Heart Circ. Physiol. 32): H1262-H1269, 1992.
29. 2+ exchange. Circ. Res. 65: 1045-1056, 1989.
30. Undrovinas, A. I., I. A. Fleidervish, and J. C. Makielski. Inward sodium current at resting potentials in single cardiac myocytes induced by the ischemic metabolite lysophosphatidylcholine. Circ. Res. 71: 1231-1241, 1992.
31. + during myocardial ischemia: consequences for post-ischemic recovery. J. Mol. Cell. Cardiol. 29: 85-96, 1997.
32. + exchanger are immediately active upon post-ischemic reperfusion in isolated rat hearts. J. Mol. Cell. Cardiol. 30: 337-348, 1998.
33. Wilde, A. A. M., and G. Aksnes. Myocardial potassium loss and cell depolarisation in ischaemia and hypoxia. Cardiovasc. Res. 29: 1-15, 1995.
34. Wu, J., and P. B. Corr. Palmitoyl carnitine modifies sodium currents and induces transient inward current in ventricular myocytes. Am. J. Physiol. 266 (Heart Circ. Physiol. 35): H1034-H1046, 1994.