β1-Adrenergic blocker bisoprolol reverses down-regulated ion channels in sinoatrial node of heart failure rats.

摘要: Bisoprolol, an antagonist of β1-adrenergic receptors, is effective in reducing the morbidity and mortality patients with heart failure (HF). It has been found that HF accompanied dysfunction sinoatrial node (SAN). However, whether bisoprolol reverses decreased SAN function how relevant ion channels change were relatively less studied. messenger RNA (mRNA) expression sodium hyperpolarization-activated cyclic nucleotide-gated (HCN) channel subunits assessed sham-operated rats, abdominal arterio-venous shunt (volume overload)-induced bisoprolol- treated rats. cells rats isolated by laser capture microdissection. Quantitative real-time PCR analysis was used to quantify mRNA HCN SAN. Intrinsic rate declined sinus recovery time prolonged indicating suppressed function, which could be improved treatment. Nav1.1, Nav1.6, HCN4 expressions reduced compared control Treatment reverse both partially. These data indicated treatment partially due reversing down-regulation (Nav1.1 Nav1.6) (HCN4) failing hearts.