Key result
Protein tyrosine kinase inhibitors significantly inhibited transient outward current in human atrial myocytes in a concentration-dependent manner, independent of serine/threonine kinases.
Why the study?
Do protein tyrosine kinase (PTK) inhibitors regulate transient outward current (I(to)) in human atrial myocytes?
Population
Human atrial myocytes isolated enzymatically from biopsies of right atrial appendage obtained from patients…
Comparison
Protein tyrosine kinase inhibitors vs Inactive analogues and baseline conditions
Design
Preclinical
Authors
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May alter atrial repolarization with PTK inhibitor use; leaves open arrhythmia risk in patients.
Do protein tyrosine kinase (PTK) inhibitors regulate transient outward current (I(to)) in human atrial myocytes?
The protein tyrosine kinase pathway plays a significant role in regulating basal transient outward current in human atrial myocytes, independent of serine/threonine kinases.
Wang et al. (2002) studied Patients undergoing coronary artery bypass surgery. Protein tyrosine kinase (PTK) inhibitors (genistein, AG957, ST638, PP2) vs. Inactive analogues (daidzein, PP3) was evaluated on Transient outward current (I(to)) amplitude and inactivation. Protein tyrosine kinase inhibitors significantly inhibited transient outward current in human atrial myocytes in a concentration-dependent manner, independent of serine/threonine kinases.
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