Angiotensin-(1–7) prevents atrial tachycardia induced-heat shock protein 27 expression

Abstract

ObjectiveWe aimed to investigate the effects of angiotensin-(1–7) [Ang-(1–7)] on heat-shock protein 27 (HSP27) in a canine model of induced tachycardia. MethodsEighteen dogs were randomized into three equal treatment groups: sham, pacing and pacing+Ang-(1–7) group. The dogs in the last two groups were subjected to 2weeks of rapid atrial pacing (500bpm). The effects of Ang-(1–7) on HSP27 were assessed by real-time polymerase chain reaction and western blot. ResultsThe expression levels of atrial HSP27 mRNA and protein were significantly (P<0.05) higher for the pacing group than the sham group and significantly (P<0.05) lower for the pacing+Ang-(1–7) group than the pacing group. There was no significant difference between the HSP27 expression levels in the right and left atria among all three groups. ConclusionsOur findings suggest that the overexpression of HSP27 may possibly be occurring as an adaptive response that allows atrial tissues to cope with rapid atrial pacing, and an inhibiting effect of Ang-(1–7) on atrial remodeling may be one of the mechanisms responsible for the attenuation of HSP27 up-regulation induced by rapid pacing.