Nitric Oxide Protects Cardiac Sarcolemmal Membrane Enzyme Function and Ion Active Transport against Ischemia-induced Inactivation
| Autor: | Shanmuga P. Kuppusamy, Hongmei Cui, Haiquan Li, Arthur L. Burnett, Paul L. Huang, Jing Q. Wang, Kai Y. Xu, Ted M. Dawson, Periannan Kuppusamy, Lewis C. Becker |
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| Rok vydání: | 2003 |
| Předmět: |
Nitric Oxide Synthase Type III
ATPase Biological Transport Active Nitric Oxide Synthase Type I In Vitro Techniques Nitric Oxide Protective Agents Biochemistry Nitric oxide Rats Sprague-Dawley chemistry.chemical_compound Sarcolemma Ion binding Ischemia medicine Animals Nitric Oxide Donors Molecular Biology Ion transporter Ion Transport biology Chemistry Myocardium Cardiac muscle Membrane Proteins Cell Biology Rats Enzyme Activation Nitric oxide synthase medicine.anatomical_structure biology.protein Biophysics Female Nitric Oxide Synthase Sodium-Potassium-Exchanging ATPase Protein Binding |
| Zdroj: | Journal of Biological Chemistry. 278:41798-41803 |
| ISSN: | 0021-9258 |
| Popis: | Nitric oxide (NO.) generated from nitric oxide synthase (NOS) isoforms bound to cellular membranes may serve to modulate oxidative stresses in cardiac muscle and thereby regulate the function of key membrane-associated enzymes. Ischemia is known to inhibit the function of sarcolemmal enzymes, including the (Na+ + K+)-ATPase, but it is unknown whether concomitant injury to sarcolemma (SL)-associated NOS isoforms may contribute to this process by reducing the availability of locally generated NO.. Here we report that nNOS, as well as eNOS (SL NOSs), are tightly associated with cardiac SL membranes in several different species. In isolated perfused rat hearts, global ischemia caused a time-dependent irreversible injury to cardiac SL NOSs and a disruption of SL NO. generation. Pretreatment with low concentrations of the NO. donor 1-hydroxy-2-oxo-3-(N-3-methyl-aminopropyl)-3-methyl-1-triazene (NOC-7) markedly protected both SL NOS and (Na+ + K+)-ATPase functions against ischemia-induced inactivation. Moreover, ischemia impaired SL Na+/K+ binding, and NOC-7 significantly prevented ischemic injury to the ion binding sites on (Na+ + K+)-ATPase. These novel findings indicate that NO. can protect cardiac SL NOSs and (Na+ + K+)-ATPase against ischemia-induced inactivation and suggest that locally generated NO. may serve to regulate SL Na+/K+ ion active transport in the heart. |
| Databáze: | OpenAIRE |
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