IP3-mediated Ca2+ release regulates atrial Ca2+ transients and pacemaker function by stimulation of adenylyl cyclases-Reference-Cited by-同舟云学术

IP3-mediated Ca2+ release regulates atrial Ca2+ transients and pacemaker function by stimulation of adenylyl cyclases

Published:2021-01-01 Issue:1 Volume:320 Page:H95-H107
ISSN:0363-6135
Container-title:American Journal of Physiology-Heart and Circulatory Physiology
language:en
Short-container-title:American Journal of Physiology-Heart and Circulatory Physiology

Author:

Capel Rebecca A.¹,Bose Samuel J.¹,Collins Thomas P.¹,Rajasundaram Skanda¹,Ayagama Thamali¹,Zaccolo Manuela²^ORCID,Burton Rebecca-Ann Beatrice¹^ORCID,Terrar Derek A.¹

Affiliation:

1. Department of Pharmacology, British Heart Foundation Centre of Research Excellence, University of Oxford, Oxford, United Kingdom

2. Department of Physiology, Anatomy and Genetics, University of Oxford, Oxford, United Kingdom

Abstract

This study provides evidence supporting the proposal that IP3 signaling in cardiac atria and sinoatrial node involves stimulation of Ca2+-activated adenylyl cyclases (AC1 and AC8) by IP3-evoked Ca2+ release from junctional sarcoplasmic reticulum. AC8 and IP3 receptors are shown to be located close together, while AC1 is nearby. Greater understanding of these novel aspects of the IP3 signal transduction mechanism is important for future study in atrial physiology and pathophysiology, particularly atrial fibrillation.

Funder

Wellcome Trust and Royal Society

Returners Carers Fund, University of Oxford

British Heart Foundation

Publisher

American Physiological Society

Subject

Physiology (medical),Cardiology and Cardiovascular Medicine,Physiology

Link

https://journals.physiology.org/doi/pdf/10.1152/ajpheart.00380.2020

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1. Cardiac excitation–contraction coupling