Abstract
Recent studies employing Ca2+ indicators and confocal microscopy demonstrate substantial local Ca2+ release beneath the cell plasma membrane (subspace) of sinoatrial node cells (SANCs) occurring during diastolic depolarization. Pharmacological and biophysical experiments have suggested that the released Ca2+ interacts with the plasma membrane via the ion current (/NaCa) produced by the Na +/Ca2+ exchanger and constitutes an important determinant of the pacemaker rate. This study provides a numerical validation of the functional importance of diastolic Ca2+ release for rate control. The subspace Ca2+ signals in rabbit SANCs were measured by laser confocal microscopy, averaged, and calibrated. The time course of the subspace [Ca2+] displayed both diastolic and systolic components. The diastolic component was mainly due to the local Ca2+ releases; it was numerically approximated and incorporated into a SANC cellular electrophysiology model. The model predicts that the diastolic Ca2+ release strongly interacts with plasma membrane via /NaCa and thus controls the phase of the action potential upstroke and ultimately the final action potential rate.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 2596-2605 |
| Number of pages | 10 |
| Journal | Biophysical Journal |
| Volume | 86 |
| Issue number | 4 |
| State | Published - Apr 2004 |
| Externally published | Yes |
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ASJC Scopus subject areas
- Biophysics
Cite this
Diastolic Calcium Release Controls the Beating Rate of Rabbit Sinoatrial Node Cells : Numerical Modeling of the Coupling Process. / Maltsev, Victor A.; Vinogradova, Tatiana M.; Bogdanov, Konstantin Y.; Lakatta, Edward; Stern, Michael D.
In: Biophysical Journal, Vol. 86, No. 4, 04.2004, p. 2596-2605.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Diastolic Calcium Release Controls the Beating Rate of Rabbit Sinoatrial Node Cells
T2 - Numerical Modeling of the Coupling Process
AU - Maltsev, Victor A.
AU - Vinogradova, Tatiana M.
AU - Bogdanov, Konstantin Y.
AU - Lakatta, Edward
AU - Stern, Michael D.
PY - 2004/4
Y1 - 2004/4
N2 - Recent studies employing Ca2+ indicators and confocal microscopy demonstrate substantial local Ca2+ release beneath the cell plasma membrane (subspace) of sinoatrial node cells (SANCs) occurring during diastolic depolarization. Pharmacological and biophysical experiments have suggested that the released Ca2+ interacts with the plasma membrane via the ion current (/NaCa) produced by the Na +/Ca2+ exchanger and constitutes an important determinant of the pacemaker rate. This study provides a numerical validation of the functional importance of diastolic Ca2+ release for rate control. The subspace Ca2+ signals in rabbit SANCs were measured by laser confocal microscopy, averaged, and calibrated. The time course of the subspace [Ca2+] displayed both diastolic and systolic components. The diastolic component was mainly due to the local Ca2+ releases; it was numerically approximated and incorporated into a SANC cellular electrophysiology model. The model predicts that the diastolic Ca2+ release strongly interacts with plasma membrane via /NaCa and thus controls the phase of the action potential upstroke and ultimately the final action potential rate.
AB - Recent studies employing Ca2+ indicators and confocal microscopy demonstrate substantial local Ca2+ release beneath the cell plasma membrane (subspace) of sinoatrial node cells (SANCs) occurring during diastolic depolarization. Pharmacological and biophysical experiments have suggested that the released Ca2+ interacts with the plasma membrane via the ion current (/NaCa) produced by the Na +/Ca2+ exchanger and constitutes an important determinant of the pacemaker rate. This study provides a numerical validation of the functional importance of diastolic Ca2+ release for rate control. The subspace Ca2+ signals in rabbit SANCs were measured by laser confocal microscopy, averaged, and calibrated. The time course of the subspace [Ca2+] displayed both diastolic and systolic components. The diastolic component was mainly due to the local Ca2+ releases; it was numerically approximated and incorporated into a SANC cellular electrophysiology model. The model predicts that the diastolic Ca2+ release strongly interacts with plasma membrane via /NaCa and thus controls the phase of the action potential upstroke and ultimately the final action potential rate.
UR - http://www.scopus.com/inward/record.url?scp=1942487269&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=1942487269&partnerID=8YFLogxK
M3 - Article
C2 - 15041695
AN - SCOPUS:1942487269
VL - 86
SP - 2596
EP - 2605
JO - Biophysical Journal
JF - Biophysical Journal
SN - 0006-3495
IS - 4
ER -