Lack of nitric oxide synthase depresses ion transporting enzyme function in cardiac muscle

Lan Zhou, Arthur L. Burnett, Paul L. Huang, Lewis C. Becker, Periannan Kuppusamy, David A. Kass, J. Kevin Donahue, David Proud, James S.K. Sham, Ted M. Dawson, Kai Y. Xu

Research output: Contribution to journalArticlepeer-review

32 Scopus citations


Nitric oxide (NO·) is produced endogenously from NOS isoforms bound to sarcolemmal (SL) and sarcoplasmic reticulum (SR) membranes. To investigate whether locally generated NO· directly affects the activity of enzymes mediating ion active transport we studied whether knockout of selected NOS isoforms would affect the functions of cardiac SL (Na+ + K+)-ATPase and SR Ca2+-ATPase. Cardiac SL and SR vesicles containing either SL (Na+ + K+)-ATPase or SR Ca2+-ATPase were isolated from mice lacking either nNOS or eNOS or both and tested for enzyme activities. Western blot analysis revealed that absence of single or double NOS isoforms did not interrupt the protein expression of SL (Na+ + K+)-ATPase and SR Ca2+-ATPase in cardiac muscle cells. However lack of NOS isoforms in cardiac muscle significantly altered both (Na+ + K+)-ATPase activity and SR Ca2+-ATPase function. Our experimental results suggest that disrupted endogenous NO· production may change local redox conditions and lead to an unbalanced free radical homeostasis in cardiac muscle cells which in turn may affect key enzyme activities and membrane ion active transport systems in the heart.

Original languageEnglish (US)
Pages (from-to)1030-1035
Number of pages6
JournalBiochemical and Biophysical Research Communications
Issue number5
StatePublished - 2002


  • (Na + K)-ATPase
  • Ca-ATPase
  • Membrane ion active transport
  • NOS knockout mice
  • Nitric oxide

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology


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