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Isoform-specific alterations in cardiac and erythrocyte Na+,K+-ATPase activity induced by norepinephrine
A Baba1, T Yoshikawa, I Nakamura
1Department of Medicine, Keio University School of Medicine, Tokyo, Japan.
Insights
Erythrocyte Na+,K+-ATPase activity mirrors myocardial enzyme activity in heart failure. This finding offers a potential clinical marker for monitoring heart function and related enzyme changes.
Area of Science:
- Biochemistry
- Cardiology
- Physiology
Background:
- Myocardial Na+,K+-ATPase activity decreases in heart failure due to elevated norepinephrine.
- Monitoring myocardial enzyme activity in clinical settings is challenging.
Purpose of the Study:
- To determine if erythrocyte Na+,K+-ATPase activity reflects myocardial enzyme activity.
- To investigate isoform-specific alterations in Na+,K+-ATPase in response to catecholamines.
Main Methods:
- Na+,K+-ATPase activity measured using a colorimetric method in rabbit myocardium and erythrocytes.
- Protein levels of Na+,K+-ATPase isoforms analyzed via Western blot.
- Norepinephrine administered to one group of rabbits; saline to controls.
Main Results:
- Norepinephrine treatment significantly reduced Na+,K+-ATPase activity in both myocardium and erythrocytes.
- A strong positive correlation (r = .963) was observed between myocardial and erythrocyte Na+,K+-ATPase activity.
- Isoform analysis revealed differences: alpha3-isoform decreased in myocardium, alpha1-isoform decreased in erythrocytes.
Conclusions:
- Erythrocyte Na+,K+-ATPase activity serves as a viable indicator of myocardial Na+,K+-ATPase activity.
- Isoform-specific regulation differs between myocardium and erythrocytes.
- Erythrocyte Na+,K+-ATPase may offer a non-invasive biomarker for heart failure.
Background:
Myocardial Na+,K+-ATPase activities are decreased in congestive heart failure because of an increase in plasma norepinephrine levels, but it is difficult to monitor the activities in the clinical setting.
Methods And Results:
This study investigated whether erythrocyte Na+,K+-ATPase activity can reflect myocardial enzyme activity and whether isoform-specific alterations occur in the presence of catecholamine. Na+,K+-ATPase activity was measured by the colorimetric method by using the left ventricular myocardium and erythrocytes prepared from eight rabbits given norepinephrine for 7 days and from eight control rabbits that received saline. The protein levels of total catalytic subunit and alpha1- or alpha3-isoform of Na+,K+-ATPase were determined by Western blot analysis. Na+,K+-ATPase activity was lower in both myocardium and erythrocytes from norepinephrine-treated rabbits than control rabbits (P < .01 and P < .01, respectively). There was a close correlation in Na+,K+-ATPase activity between myocardium and erythrocytes (r = .963). Total catalytic subunit protein level was lower in myocardium from norepinephrine-treated rabbits than control rabbits, but the alpha1-isoform level was similar between the two groups. The alpha3-isoform level was lower in norepinephrine-treated rabbits than control rabbits. In erythrocytes, alpha1-isoform was lower in norepinephrine-treated rabbits than control rabbits.
Conclusions:
Na+,K+-ATPase activity in myocardium could be reflected in erythrocyte membrane, although there was a difference in isoform-specific regulation between the two.