Sarcoplasmic Reticulum Ca 2+ Pumping Kinetics Regulates Timing of Local Ca 2+ Releases and Spontaneous Beating Rate of Rabbit Sinoatrial Node Pacemaker Cells | Zendy

Tatiana M. Vinogradova | Zendy; Didier X.P. Brochet | Zendy; Syevda Sirenko | Zendy; Yue Li | Zendy; Harold A. Spurgeon | Zendy; Edward G. Lakatta | Zendy

Open Access

Sarcoplasmic Reticulum Ca ²⁺ Pumping Kinetics Regulates Timing of Local Ca ²⁺ Releases and Spontaneous Beating Rate of Rabbit Sinoatrial Node Pacemaker Cells

Author(s) -

Tatiana M. Vinogradova,

Didier X.P. Brochet,

Syevda Sirenko,

Yue Li,

Harold A. Spurgeon,

Edward G. Lakatta

Publication year - 2010

Publication title -

circulation research

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 4.899

H-Index - 336

eISSN - 1524-4571

pISSN - 0009-7330

DOI - 10.1161/circresaha.110.220517

Subject(s) - cyclopiazonic acid , phospholamban , sinoatrial node , endoplasmic reticulum , diastolic depolarization , biophysics , depolarization , chemistry , cytosol , calcium , medicine , endocrinology , biochemistry , biology , heart rate , enzyme , organic chemistry , blood pressure

Sinoatrial node cells (SANCs) generate local, subsarcolemmal Ca(2+) releases (LCRs) from sarcoplasmic reticulum (SR) during late diastolic depolarization. LCRs activate an inward Na(+)-Ca(2+) exchange current (I(NCX)), which accelerates diastolic depolarization rate, prompting the next action potential (AP). The LCR period, ie, a delay between AP-induced Ca(2+) transient and LCR appearance, defines the time of late diastolic depolarization I(NCX) activation. Mechanisms that control the LCR period, however, are still unidentified.

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