February 3, 2004The Journal of PhysiologyOpen Access

Inositol‐1,4,5‐trisphosphate‐dependent Ca2+ signalling in cat atrial excitation–contraction coupling and arrhythmias

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Population

Intact and saponin-permeabilized cat atrial myocytes

Comparison

Endothelin, IP3, and adenophostin with or… vs Control conditions (absence of agonists/blockers)

Design

Preclinical

Authors

AZAleksey V. ZimaLoyola University Chicago LBLothar A. BlatterElectrophysiology

Discussion

Member takes

Implication

Hypothesis-generating for IP3-mediated atrial Ca2+ dysregulation in AF; does not yet support clinical interventions.

Structured PICO

Population

Intact and saponin-permeabilized cat atrial myocytes

Intervention

Endothelin (ET-1), IP3, and adenophostin with or without IP3 receptor blockers (2-APB, heparin) or RyR blocker (tetracaine)

Comparator

Control conditions (absence of agonists/blockers)

Outcome

Intracellular Ca2+ levels, Ca2+ transients, Ca2+ sparks, and arrhythmogenic Ca2+ wavessurrogate

IP3-dependent Ca2+ release plays a significant role in atrial excitation-contraction coupling and may contribute to the development of Ca2+-mediated atrial arrhythmias.

Cite This Study

Zima et al. (2004) studied this question.

synapsesocial.com/papers/69eedfafa84321e0ae63c873 https://doi.org/10.1113/jphysiol.2003.058529

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Bookmark

Inositol‐1,4,5‐trisphosphate‐dependent Ca2+ signalling in cat atrial excitation–contraction coupling and arrhythmias

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Inositol‐1,4,5‐trisphosphate‐dependent Ca2+ signalling in cat atrial excitation–contraction coupling and arrhythmias

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Also Consider

Also Consider