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Updated: Oct 1, 2026

Isolation of Human Atrial Myocytes for Simultaneous Measurements of Ca2+ Transients and Membrane Currents
Published on: July 3, 2013
Attenuation of negatively regulated ANP secretion by calcium in hypertrophied atria
Suhn Hee Kim1, Chunhua Cao, Jeong Hee Han
1Department of Physiology, Medical School, Institute for Medical Sciences, Jeonbug National University, 2-20 Keum-Am-Dong-San, Jeonju 560-180, South Korea. shkim@moak.chonbuk.ac.kr
Insights
Cardiac hypertrophy impairs atrial natriuretic peptide (ANP) secretion regulation by calcium. Hypertrophied atria show reduced responsiveness to calcium depletion, suggesting disrupted intracellular calcium handling affects ANP release.
Area of Science:
- Cardiovascular Physiology
- Cellular Biology
- Endocrinology
Background:
- Abnormal intracellular calcium handling is linked to heart diseases and cardiac hypertrophy.
- The precise role of calcium in atrial cardiomyocyte excitation-secretion coupling remains unclear.
- Atrial natriuretic peptide (ANP) secretion is crucial for cardiovascular homeostasis.
Purpose of the Study:
- To investigate how calcium modulates atrial natriuretic peptide (ANP) secretion in hypertrophied atria.
- To determine the responsiveness of stretch-induced ANP secretion to calcium variations in cardiac hypertrophy.
- To elucidate the impact of altered intracellular calcium regulation on ANP secretion in hypertrophied atrial tissue.
Main Methods:
- Utilized isolated perfused quiescent hypertrophied rat atria induced by monocrotaline (MCT) injection.
- Studied mechanically stimulated extracellular fluid (ECF) translocation and stretch-induced ANP secretion.
- Assessed the effects of extracellular calcium depletion on ANP secretion and intracellular calcium levels in atrial myocytes.
Main Results:
- Increased atrial volume led to proportional increases in ECF translocation and stretch-induced ANP secretion.
- Extracellular calcium depletion markedly increased ANP secretion in control atria but this effect was attenuated in hypertrophied atria.
- Hypertrophied atrial myocytes exhibited attenuated decreases in intracellular calcium upon extracellular calcium depletion compared to control myocytes.
Conclusions:
- Stretch-induced ANP secretion in hypertrophied atria is less responsive to extracellular calcium depletion.
- Disturbances in intracellular calcium regulation in hypertrophied atria likely contribute to the attenuated negative regulation of ANP secretion.
- These findings highlight altered calcium handling as a key factor in abnormal ANP secretion during cardiac hypertrophy.
Abstract:
Abnormal intracellular Ca(2+)-handling has been described in various heart diseases associated with cardiac hypertrophy. The crucial role of Ca(2+) in the excitation-secretion coupling in atrial cardiomyocytes is not well established. To investigate modulation of atrial natriuretic peptide (ANP) secretion regulated by Ca(2+) in hypertrophied atria, responsiveness of stretch-induced ANP to Ca(2+) was studied using isolated perfused quiescent hypertrophied rat atria. Male Sprague-Dawley rats were given a single subcutaneous injection of 50 mg/kg monocrotaline (MCT) and were sacrificed at 5-6 weeks. In isolated perfused hypertrophied right atria from MCT rats, changes in atrial volume induced by increased atrial pressure caused proportional increases in mechanically stimulated extracellular fluid (ECF) translocation and stretch-induced ANP secretion. Stretch-induced ANP secretion was markedly increased by the depletion of extracellular Ca(2+). However, an accentuation of stretch-induced ANP secretion by Ca(2+) depletion was markedly attenuated in hypertrophied right atria, as compared to control right atria. Therefore, stretch-induced ANP secretion in terms of ECF translocation by Ca(2+) depletion in hypertrophied atria was significantly lower than in control right atria. However, no significant differences were observed between nonhypertrophied and control left atria. Depletion of extracellular Ca(2+) caused a decrease in intracellular calcium in single beating atrial myocytes, which was significantly attenuated in hypertrophied atrial myocytes. The results suggest that attenuation of Ca(2+)-induced negative regulation of ANP secretion in hypertrophied atria may be due to the disturbance of intracellular Ca(2+) regulation.
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