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Thyroid hormone increases pacemaker activity in rat neonatal atrial myocytes.
Z Q Sun1, K Ojamaa, T Y Nakamura
1Pediatric Cardiology, NYU School of Medicine, New York, NY 10016, USA.
Journal of Molecular and Cellular Cardiology
|March 29, 2001
Summary
Thyroid hormone (T3) significantly increases heart pacemaker cell beating rates by enhancing diastolic depolarization. This effect is partly due to increased sodium-calcium exchanger activity, boosting heart rhythm regulation.
Area of Science:
- Cardiology
- Endocrinology
- Molecular Biology
Background:
- Thyroid hormones are crucial regulators of metabolism and development.
- Pacemaker activity in the heart dictates heart rate and rhythm.
- The specific electrophysiological mechanisms by which thyroid hormone influences pacemaker activity are not fully elucidated.
Purpose of the Study:
- To investigate the effects of thyroid hormone (T3) on the electrophysiological properties of neonatal rat atrial myocytes.
- To determine the impact of T3 on pacemaker activity and ion channel function.
Main Methods:
- Primary atrial myocytes were isolated from 2-day-old rats and cultured.
- Electrophysiological techniques, including voltage clamp, were used to record action potentials and ion currents.
- Cells were treated with 3,3',5-triiodo-L-thyronine (T3) at 10(-8)m for 24-48 hours.
Main Results:
- T3 treatment significantly increased the beating rate of myocytes (244+/-19 vs 122+/-10 beats/min).
- T3 enhanced the rate of diastolic depolarization, a key determinant of pacemaker activity.
- T3 increased the density of the pacemaker current (I(f)) and the Na+-Ca2+ exchanger current (I(Na/Ca)).
Conclusions:
- Thyroid hormone (T3) exerts a positive chronotropic effect on cardiac pacemaker cells.
- Increased diastolic depolarization rate and enhanced ion currents (I(f) and I(Na/Ca)) contribute to T3-induced acceleration of heart rate.
- The Na+-Ca2+ exchanger plays a significant role in mediating the effects of thyroid hormone on pacemaker activity.