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Updated: Aug 10, 2026
Isolation of Human Atrial Myocytes for Simultaneous Measurements of Ca2+ Transients and Membrane Currents
Published on: July 3, 2013
Transmembrane chloride currents in human atrial myocytes
Insights
Human atrial cells do not exhibit basal or cyclic adenosine monophosphate-dependent chloride currents. However, they do show a significant chloride conductance when cell volume increases due to swelling.
Area of Science:
- Cardiovascular Physiology
- Cellular Electrophysiology
Background:
- Chloride (Cl-) currents play crucial roles in cardiac function.
- Understanding Cl- channel activity in human atrial myocytes is vital for cardiac research.
Purpose of the Study:
- To investigate the presence of basal, swelling-induced, and cyclic adenosine monophosphate (cAMP)-dependent Cl- currents in human atrial myocytes.
- To characterize the properties of these currents using electrophysiological techniques.
Main Methods:
- Whole-cell patch-clamp technique applied to human atrial myocytes.
- Stimulation with isoproterenol, forskolin, and 8-bromoadenosine 3',5'-cyclic monophosphate.
- Induction of cell swelling using hyposmotic solutions.
- Assessment of Cl- channel blocker sensitivity and ion selectivity.
Main Results:
- No basal or cAMP-dependent Cl- currents were detected in human atrial myocytes.
- Isoproterenol and forskolin did not alter membrane conductance.
- Hyposmotic swelling induced a significant, outwardly rectifying Cl- conductance.
- This swelling-induced conductance was inhibited by 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid and showed selective Cl- permeability.
Conclusions:
- Human atrial cells lack basal and cAMP-modulated Cl- currents.
- A distinct swelling-activated Cl- conductance is present in human atrial myocytes.
- This finding suggests a role for volume-regulated Cl- channels in atrial physiology.
Abstract:
The present study was designed to evaluate the presence of basal, swelling-induced, and cAMP-dependent Cl- currents in human atrial myocytes studied with the whole cell patch-clamp technique. Under basal conditions, a small outwardly rectifying background conductance was noted that reversed close to 0 mV and was not altered by Cl- replacement. Isoproterenol (1 microM), forskolin (3 microM), and 8-bromoadenosine 3',5'-cyclic monophosphate (50 microM) did not increase membrane conductance, even when responsiveness to isoproterenol was confirmed by an increase in Ca2+ current and when perforated-patch techniques (nystatin) were used. Exposure to hyposmotic solutions increased cell volume and induced a whole cell conductance that showed outward rectification, was inhibited by 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (100 microM), and responded to changes in Cl- gradient in a fashion consistent with a Cl(-)-selective conductance, with estimated relative permeabilities of 1, 0.25, and 0.07 for Cl-, methanesulfonate, and aspartate, respectively. The results suggest that human atrial cells lack basal and adenosine 3',5'-cyclic monophosphate-dependent Cl- current but manifest a substantial Cl- conductance in the presence of cell swelling.
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