Cardiac T-type Ca2+ channels in the heart

Pituitary Adenylate Cyclase-activating Peptide (PACAP) Recruits Low Voltage-activated T-type Calcium Influx under Acute Sympathetic Stimulation in Mouse Adrenal Chromaffin Cells

“…Low voltage-activated T-type calcium channels (Ca v 3.1-3.3) have been shown to play a role in regulating the activity of excitable cells, and they are present in excitable tissues as diverse as neurons, neuroendocrine cells, and cardiac myocytes (31)(32)(33)(34)(35)(36)(37)(38). T-type Ca v 3.2 channels are pharmacologically characterized by their selective block by micromolar concentrations of nickel chloride (39).…”

Eps15 Homology Domain-containing Protein 3 Regulates Cardiac T-type Ca2+ Channel Targeting and Function in the Atria

“…1B, p Ͻ 0.01). Although the depolarization phase of the atrial action potential is primarily mediated by the voltage-gated sodium channel, Na V 1.5, the T-type calcium current may also facilitate this process (21,39). Furthermore, T-type calcium current is dysregulated in cardiac disease and linked with the maladaptive hypertrophic response associated with heart failure (40 -42).…”

“…Although not enriched in ventricle, the vertebrate atria expresses two TTCC gene products Ca V 3.1 (Cacna1g) and Ca V 3.2 (Cacna1h) (21). The dominant isoform in the adult atria is Ca V 3.1, whereas Ca V 3.2 is linked with embryonic and postnatal cardiac development (43).…”

“…Ca V 3.1 and Ca V 3.2 are critical mediators of action potential initiation and conduction from the sinoatrial node through the atria and into the atrioventricular node (AVN) in heart (21,22). Using a cardiac-selective model of EHD3 deficiency, we demonstrate defects in Ca V 3.1 and Ca V 3.2 expression, localization, and function in EHD3 Ϫ/Ϫ atrial myocytes.…”

The Functional Role of Chloride Channels in Cardiac Pacemaker Activity

“…The ionic mechanisms of the pacemaker activity have been one of the central research subjects in cardiac electrophysiology (DiFrancesco, 2010). It is generally agreed now that multiple mechanisms such as the hyperpolarization-activated non-selective cationic "funny" current (I f ) (DiFrancesco, 2010),the L-type (I Ca,L ) (Kurata et al, 2003) and T-type Ca 2+ currents (I Ca,T ) (Ono & Iijima, 2010), Na + /Ca 2+ exchanger (I NCX ) , and a sustained inward current (I st ) (Shinagawa et al, 2000), may be involved in the generation and regulation of spontaneous pacemaker activity, although the relative contribution of these individual ionic currents are still under debate. Early studies using ion-substitution strategies in multicellualr Purkinje fibers and SAN tissues provided initial experimental evidence for the potential physiological role of Cl -and other anions in the regulation of membrane potentials, the diastolic depolarization and action potential duration of cardiac cells (Carmeliet, 1961;Hutter & Noble, 1961;De Mello, 1963;Noma & Irisawa, 1976).…”