Nitric Oxide modulates spontaneous Ca2+ release and ventricular arrhythmias during β-adrenergic signalling through S-nitrosylation of Calcium/Calmodulin dependent kinase II

About this item

Title

Nitric Oxide modulates spontaneous Ca2+ release and ventricular arrhythmias during β-adrenergic signalling through S-nitrosylation of Calcium/Calmodulin dependent kinase II

Content partner

University of Otago

Collection

Otago University Research Archive

Description

Rationale: Nitric oxide (NO) has been identified as a signalling molecule generated during β-adrenergic receptor (AR) stimulation in the heart. Furthermore, a role for NO in triggering spontaneous Ca2+ release via S-nitrosylation of Ca2+/calmodulin kinase II delta (CaMKIIδ) is emerging. NO donors are routinely used clinically for their cardioprotective effects in the heart, but it is unknown how NO donors modulate the pro-arrhythmic CaMKII to alter cardiac arrhythmia incidence.

Format

Research paper

Research format

Scholarly text / Journal article

Thesis level

Preprint

Date created

2023-08-24

Creator

Power, Amelia S / Asamudo, Esther / Worthington, Luke P I / Alim, Chidera C / Parackal, Raquel / Wallace, Rachel S / Ebenebe, Obialunanma V / Brown, Joan Heller / Kohr, Mark J / Bers, Donald M / Erickson, Jeffrey R

URL

https://hdl.handle.net/10523/42880

Related subjects

CaMKII / Calcium / S-nitrosylation / Arrhythmias

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