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- W2295087188 abstract "Our prior work has shown that TTX-sensitive sodium current (INa) affects sarcoplasmic reticular (SR) Ca release. This current activates early reverse NCX. The resulting Ca entry primes the dyadic cleft, which appears to increase Ca channel coupling fidelity (we refer to this as the priming mechanism). The skeletal isoform Nav1.4 is the main TTX-sensitive Na channel expressed in adult rabbit ventricular cardiomyocytes. Here we tested the hypothesis that this is the principal isoform involved in the priming mechanism. We evoked action potentials (AP) in isolated rabbit ventricular cells loaded with fluo-4, and simultaneously recorded Ca transients before and after the application of either relatively low doses of TTX (100 nM) or the specific Nav1.4 inhibitor μ-Conotoxin GIIIB (1 μM). 100 nM of TTX will effectively block all skeletal and the neuronal Navs (Nav1.1 is also present with a low level of expression). However this concentration will have a negligible (5%) effect on the cardiac isoform. There was a more prominent AP upstroke velocity reduction in TTX (73±1%, n=4) than in GIIB (81±1%, n=6, P<0.05). This can be expected given the relative contribution of each Nav isoform to the phase 0 of the AP. However, the effects of either drug on SR Ca release (measured as the transient maximum upstroke velocity) were identical (69±0.03% in TTX (n=5) vs. 69±3% in GIIIB (n=6), P<0.05). Furthermore, this reduction in SR Ca release is comparable to the value that we obtained previously when total INa was inactivated with a ramp. This result suggests that the Nav skeletal isoform is the main Nav isoform involved in regulating the efficiency of excitation-contraction coupling in rabbit cardiomyocytes." @default.
- W2295087188 created "2016-06-24" @default.
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- W2295087188 date "2016-02-01" @default.
- W2295087188 modified "2023-09-28" @default.
- W2295087188 title "Activation of Reverse Na/Ca Exchanger by Skeletal Na Channel Isoform Increases Excitation-Contraction Coupling Efficiency in Rabbit Cardiomyocytes" @default.
- W2295087188 doi "https://doi.org/10.1016/j.bpj.2015.11.599" @default.
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