Effect Of Aconitine-Induced Atrial Fibrillation On Endothelin-1 Secretion And Its Receptors Expression

Atrial fibrillation (AF) is an abnormal heart rhythm characterized by rapid and irregular beating. It is recognized that AF is one of common clinical heart disease and harm to human health. The incidence of atrial fibrillation commonly increases along with aging. The mechanism of AF occurrence and maintenance is most complex. The intense research of AF focuses on its pathogenesis process and proper treatment. Although the phenomenon of atrial functional disorder including atrial structural and electrical remodeling are correlated with AF, but its detailed mechanisms are remain to be define.Endouthelin-1 (ET-1) is a potent vasoconstrictor that is recognized as an important factor for maintaining vascular tension and cardiovascular functions. The abnormal of ET-1 secretion is closely related with several cardiovascular diseases. However, it is unclear whether pathogenesis of AF is associated with ET-1 and its downstream signal mechanisms are not well known. Therefore, purpose of the present study is to investigate effect of aconitine-induced acute AF on the regulation of atrial ET-1 secretion and its receptors as well as its downstream signal molecules expressions in isolated perfused beating rat atria.The results of the present study showed that:1. Aconitine (20 nmol/L) induced atrial arhythmia at about 5 minutes after by its treatment.2. Connexin 40 and 43 expressions were significantly down regulated by aconitine-induced acute AF (P<0.01 vs. control).3. Aconitine-induced AF markedly increased atrial ET-1 secretion (P<0.001 vs. control period).4. AF induced up regulation of ETRA expression (P<0.05 vs. control group) and down regulationof ETRB expression (P<0.01 vs. control group). 5. MAPK/ERK(P<0.01 vs. control goup) and PI3K activities were obviouslyelevated by acute AF (P<0.01 vs. control goup).Results of the present study indicated that:Aconitine-induced acute AF significantly increased atrial ET-1 secretion and leaded to abnormal expressions of ET receptors as well as its down stream signal molecules and which may be correlated with AF-induced atrial structural remodeling.