Myocardial RAD Deletion Increases Early L-type Calcium Current without Affecting Late Calcium Current through Multiple Mechanisms
نویسندگان
چکیده
منابع مشابه
Rad GTPase Deletion Increases L‐type Calcium Channel Current Leading to Increased Cardiac Contraction
BACKGROUND The small GTPase Rad is a negative regulator of voltage-dependent L-type calcium channel current (ICaL); however, the effects of Rad ablation on cardiomyocyte function are unknown. The objective of this study is to test the hypothesis that Rad-depletion causes positive inotropic effects without inducing cardiac hypertrophy. METHODS AND RESULTS Ventricular myocytes from adult Rad(-/...
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We have examined slow inactivation of L-type calcium current in canine Purkinje myocytes with the whole cell patch clamp technique. Slow inactivation is voltage dependent. It is negligible at -50 mV but can inactivate more than half of available iCaL at -10 mV. There are two major consequences of this slow inactivation. First, standard protocols for the measurement of T-type current can dramati...
متن کاملSlow Inactivation of L-Type Calcium Current Distorts the Measurement of L- and T-Type Calcium Current in Purkinje Myocytes
We have examined slow inactivation of L-type calcium current in canine Purkinje myocytes with the whole cell patch clamp technique. Slow inactivation is voltage dependent. It is negligible at -50 mV but can inactivate more than half of available icaL at 1 0 inV. There are two major consequences of this slow inactivation. First, standard protocols for the measurement of T-type current can dramat...
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Effects of haloperidol on L-type CaV1.2 channel were studied. Calcium current was measured in whole cell patch-clamp using calcium as a charge carrier. Inhibition by haloperidol was investigated in CaV1.2 channel natively expressed in rat cardiac myocytes and recombinant cardiac (CaV1.2a) and vascular (CaV1.2b) splice variants of the channel expressed in HEK 293 cells. Haloperidol inhibited L-t...
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ژورنال
عنوان ژورنال: Biophysical Journal
سال: 2020
ISSN: 0006-3495
DOI: 10.1016/j.bpj.2019.11.726