English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Coupling of an intracellular Ca 2+  clock to surface membrane ion channels, i.e., a “membrane clock, ” via coupling of electrochemical Na +  and Ca 2+  gradients ( E Na  and E Ca , respectively) has been theorized to regulate sinoatrial nodal cell (SANC) normal automaticity. To test this hypothesis, we measured responses of [Na + ] i , [Ca 2+ ] i , membrane potential, action potential cycle length (APCL), and rhythm in rabbit SANCs to Na + /K +  pump inhibition by the digitalis glycoside, digoxigenin (DG, 10–20 μmol/l). Initial small but significant increases in [Na + ] i  and [Ca 2+ ] i  and reductions in E Na  and E Ca  in response to DG led to a small reduction in maximum diastolic potential (MDP), significantly enhanced local diastolic Ca 2+  releases (LCRs), and reduced the average APCL. As [Na + ] i  and [Ca 2+ ] i  continued to increase at longer times following DG exposure, further significant reductions in MDP, E Na , and E Ca  occurred; LCRs became significantly reduced, and APCL became progressively and significantly prolonged. This was accompanied by increased APCL variability. We also employed a coupled-clock numerical model to simulate changes in E Na  and E Ca  simultaneously with ion currents not measured experimentally. Numerical modeling predicted that, as the E Na  and E Ca  monotonically reduced over time in response to DG, ion currents ( I CaL , I CaT , I f , I Kr , and I bNa ) monotonically decreased. In parallel with the biphasic APCL, diastolic I NCX  manifested biphasic changes; initial I NCX  increase attributable to enhanced LCR ensemble Ca 2+  signal was followed by I NCX  reduction as E NCX  ( E NCX  = 3 E Na  − 2 E Ca ) decreased. Thus SANC automaticity is tightly regulated by E Na , E Ca , and E NCX  via a complex interplay of numerous key clock components that regulate SANC clock coupling.

american journal of physiology. heart and circulatory physiology

Electrochemical Na<sup>+</sup> and Ca<sup>2+</sup> gradients drive coupled-clock regulation of automaticity of isolated rabbit sinoatrial nodal pacemaker cells

Electrochemical Na+ and Ca2+ gradients drive coupled-clock regulation of automaticity of isolated rabbit sinoatrial nodal pacemaker cells

Electrochemical Na⁺ and Ca²⁺ gradients drive coupled-clock regulation of automaticity of isolated rabbit sinoatrial nodal pacemaker cells