Inhibition of G protein-gated K⁺ channels by tertiapin-Q rescues sinus node dysfunction and atrioventricular conduction in mouse models of primary bradycardia.

ABSTRACT: Sinus node (SAN) dysfunction (SND) manifests as low heart rate (HR) and is often accompanied by atrial tachycardia or atrioventricular (AV) block. The only currently available therapy for chronic SND is the implantation of an electronic pacemaker. Because of the growing burden of SND in the population, new pharmacological therapies of chronic SND and heart block are desirable. We developed a collection of genetically modified mouse strains recapitulating human primary SND associated with different degrees of AV block. These mice were generated with genetic ablation of L-type Ca_v1.3 (Ca_v1.3^-/-), T-type Ca_v3.1 (Ca_v3.1^-/-), or both (Ca_v1.3^-/-/Ca_v3.1^-/-). We also studied mice haplo-ins

SUBMITTER: Bidaud I 

PROVIDER: S-EPMC7300035 | biostudies-literature | 2020 Jun

REPOSITORIES: biostudies-literature