Abstract:
OBJECTIVE:We have recently identified an activation site on (Na+ + K+)-ATPase and found that binding of antibody SSA412 to this specific site of the enzyme markedly augments (Na+ + K+)-ATPase catalytic activity. Demonstration of whether activation of (Na+ + K+)-ATPase affects heart function in animal in vivo was the object of this investigation. METHODS:Male wild-type CD-1 mouse and specific antibody SSA412 were used for the study. A pressure-volume micromanometer-conductance catheter in anesthetized mouse assessed in vivo cardiac functions. RESULTS:Specific antibody SSA412 infusion in mouse shifted pressure-volume loop leftward with increased stroke volume and enhanced end-systolic elastance. Global systolic parameters such as ejection fraction and cardiac output, and load independent contractile parameters including dP/dtmax/IP, PMX/EDV, Ees, and PRSW, were all increased without any effect on relaxation following administration of SSA412. Cardiac preload indexed by EDV and afterload by ESP did not alter, suggesting that SSA412-enhanced myocardial performance is a direct cardiac effect caused by the activation of (Na+ + K+)-ATPase. CONCLUSION:Our study provides the first in vivo physiological evidence to demonstrate that activation of (Na+ + K+)-ATPase induces significant positive inotropic effect in intact animal heart. The finding may lead to new therapeutic strategies for the treatment of heart failure.
journal_name
Biochem Biophys Res Communjournal_title
Biochemical and biophysical research communicationsauthors
Xu KY,Takimoto E,Fedarko NSdoi
10.1016/j.bbrc.2006.08.070subject
Has Abstractpub_date
2006-10-20 00:00:00pages
582-7issue
2eissn
0006-291Xissn
1090-2104pii
S0006-291X(06)01870-5journal_volume
349pub_type
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