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Ambulatory ECG Recording in Mice
Published on: May 27, 2010
Surface electrocardiogram and action potential in mice lacking urea transporter UT-B
Yan Meng1, Chunyan Zhao, Xuexin Zhang
1Department of Pathophysiology, School of Basic Medicine, Jilin University, Changchun, 130021, China.
Science in China. Series C, Life Sciences
|May 28, 2009
Summary
Deletion of urea transporter UT-B in mice leads to progressive heart block. This study reveals UT-B
Area of Science:
- Cardiology
- Physiology
- Molecular Biology
Background:
- Urea transporter UT-B is expressed in various tissues, including the heart.
- The specific role of UT-B in cardiac function is not well understood.
Purpose of the Study:
- To investigate the cardiac phenotype associated with UT-B deletion in mice.
- To determine the impact of UT-B absence on heart electrophysiology and function.
Main Methods:
- RT-PCR and Western blot to confirm UT-B expression in wild-type and null mice.
- Surface electrocardiogram (ECG) recordings in mice at multiple ages.
- Electrophysiological studies including action potential and sodium current recordings in isolated ventricular myocytes.
Main Results:
- UT-B expression was confirmed in wild-type mouse hearts, absent in null mice.
- UT-B null mice exhibited significantly prolonged P-R intervals and developed age-dependent heart block (Types II and III).
- Cardiac electrophysiology was altered, showing decreased action potential amplitude and Vmax, prolonged action potential duration, and reduced maximal sodium current in UT-B null mice.
Conclusions:
- UT-B deletion in mice results in progressive cardiac conduction defects and heart block.
- These findings highlight a critical role for UT-B in maintaining normal cardiac electrical activity.
- The study provides the first evidence linking UT-B deficiency to cardiac dysfunction and heart block.

