The Calcium and Voltage Clocks in Sinoatrial Node Automaticity.
10.4070/kcj.2009.39.6.217
- Author:
Boyoung JOUNG
1
;
Masahiro OGAWA
;
Shien Fong LIN
;
Peng Sheng CHEN
Author Information
1. Krannert Institute of Cardiology and the Division of Cardiology, Department of Medicine, Indiana University School of Medicine, Indianapolis, USA. chenpp@iupui.edu
- Publication Type:Review
- Keywords:
Calcium;
Sinoatrial node;
Sarcoplasmic reticulum;
Sympathetic nervous system
- MeSH:
Action Potentials;
Calcium;
Heart Rate;
Membrane Potentials;
Membranes;
Sarcoplasmic Reticulum;
Sinoatrial Node;
Sympathetic Nervous System
- From:Korean Circulation Journal
2009;39(6):217-222
- CountryRepublic of Korea
- Language:English
-
Abstract:
Recent evidence indicates that the voltage (cyclic activation and deactivation of membrane ion channels) and Ca2+ clocks (rhythmic spontaneous sarcoplasmic reticulum Ca2+ release) jointly regulate sinoatrial node (SAN) automaticity. Since the intact SAN is a heterogeneous structure that includes multiple different cell types interacting with each other, the relative importance of the voltage and Ca2+ clocks for pacemaking may be variable in different regions of the SAN. Recently, we performed optical mapping in isolated and Langendorff-perfused canine right atria. We mapped the intracellular calcium (Cai) and membrane potentials of the intact SAN simultaneously. Using previously described criteria of the timing of the late diastolic Cai elevation (LDCAE) relative to the action potential upstroke to detect Ca2+ clock activity, we demonstrated that the sinus rate increased and the leading pacemaker shifted to the superior SAN with the robust LDCAE during beta-adrenergic stimulation. We also showed that the LDCAE was caused by spontaneous diastolic SR Ca2+ release and was closely related with heart rate changes. We conclude that the Ca2+ and voltage clocks work synergistically to generate SAN automaticity.
