Table 1.

Characteristics of the L- and T-type VGCCs isoforms involved in cardiac automaticity.

	L-type VGCC (Cav1)		T-type VGCC (Cav3)
	Cav1.2	Cav1.3	Cav3.1	Cav3.2
Expression time	Embryonic stage	Embryonic stage	Start to increase in the perinatal period and becomes predominant in the adulthood	High in Embryonic heart tissue and then decrease and disappear in adult heart
Cardiac tissues expression	SAN, AVN, atria, PF networks, Ventricles	SAN, AVN, atria, PF networks, poorly or not expressed in ventricular	SAN, AVN, atria, PF networks, poorly or not expressed in ventricular tissue	SAN, AVN, atria, PF networks, poorly expressed in ventricular tissue
Voltage dependent activation	High threshold of activation (~−40 mV) Fast activation	Lower threshold of activation than Cav1.2 (~−55 mV) Fast activation	Lower threshold of activation (~−70 mV) Slow activation
Inactivation properties	Ca2+ and voltage dependent inactivation	Ca2+ and voltage dependent inactivation	Fast voltage dependent inactivation
DHP sensitivity	High	Lower than Cav1.2	Low and very low
Role in pacemaking	Control the Ca2+ dependent upstroke phase of action potential	Diastolic pacemaker current	Diastolic pacemaker current
Knock-out mice phenotype	Lethal	Strong bradycardia, SAN arrhythmia, conduction system dysfunction	Mild bradycardia AV conduction disorders	No phenotype