TY - JOUR
AU - Urthaler, Ferdinand
AB - excitable cells through the Orai calcium channels 6. Wolkowicz PE, Huang J, Umeda PK, Sharifov OF, they would so decrease conduction velocity with EC s identical to those that cause cardiac 1 Tabengwa E, Halloran BA et al. Pharmacological evi- and provoke re-entry. Electromechanical ectopy. These channels, and the related transi- dence for Orai channel activation as a source of uncouplers and voltage-sensitive dyes them- ent receptor potential proteins, are important cardiac abnormal automaticity. Eur J Pharm 2011; 11,12 selves decrease impulse conduction. This regulators of cell calcium signalling. Huo pub- 668:208 – 216. 7. Wolkowicz PE, Umeda PK, Urthaler F, Sharifov OF. may contribute to the low conduction Bingen lished that 2APB activates calcium entry in iso- 8 Voltage-independent calcium channels, molecular reports at doses of 2APB that do not greatly lated myocytes ; we reported that Orai sources of supraventricular arrhythmia. In: Liu T, Li G, affect connexins. inhibitors suppress 2APB ectopy and that rat Korantzopoulos P, eds. Atrial Fibrillation. Rijeka, Croatia: Secondly, Bingen’s voltage-mapping studies left atria and ventricles express Orai1 and InTech Publishing; 2013. http://www.intechopen.com/ 2,5,6 books/atrial-fibrillation-mechanisms-and-treatment/ expand our data which demonstrated that Orai3. Thus the activation of these channels voltage-independent-calcium-channels-molecular- Bay K 8644 induces 
TI - Prolongation of minimal action potential duration in sustained fibrillation decreases complexity by transient destabilization
JO - Cardiovascular Research
DO - 10.1093/cvr/cvt022
DA - 2013-04-01
UR - https://www.deepdyve.com/lp/oxford-university-press/prolongation-of-minimal-action-potential-duration-in-sustained-Lubce5mf2j
SP - 155
EP - 156
VL - 98
IS - 1
DP - DeepDyve
ER -