<i>Scn1b</i> expression in the adult mouse heart modulates Na<sup>+</sup> influx in myocytes and reveals a mechanistic link between Na<sup>+</sup> entry and diastolic function
Daniel O. Cervantes, Emanuele Pizzo, Harshada Ketkar, Sreema P. Parambath, Samantha Tang, Eleonora Cianflone, Antonio Cannatà, Govindaiah Vinukonda, Sudhir Jain, Jason T. Jacobson, Marcello Rota
Abstract
We have investigated the consequences of deletion of Scn1b, the gene encoding voltage-gated sodium channel β1-subunits, on myocyte and cardiac function. Our findings support the notion that Scn1b expression controls properties of Na + influx and Ca 2+ cycling in cardiomyocytes affecting the modality of cell contraction and relaxation. These effects at the cellular level condition electrical recovery and diastolic function in vivo, substantiating the multifunctional role of β1-subunits in the physiology of the heart.
Topics & Concepts
MyocyteSodium channelDiastoleInternal medicineBiologyCell biologyEndocrinologyChemistryMedicineSodiumBlood pressureOrganic chemistryCardiac electrophysiology and arrhythmiasIon channel regulation and functionNeuroscience and Neural Engineering