Effect of heat stress on angiotensinⅡ expression in rat myocardium and its relationship to p22phox[J]. Chinese Heart Journal, 2009, 21(3): 304-308.
    Citation: Effect of heat stress on angiotensinⅡ expression in rat myocardium and its relationship to p22phox[J]. Chinese Heart Journal, 2009, 21(3): 304-308.

    Effect of heat stress on angiotensinⅡ expression in rat myocardium and its relationship to p22phox

    • AIM To study the effect of heat stress on the expression of angiotensinⅡ(AngⅡ) in the myocardium and to investigate the interrelation between AngⅡ and p22phox in the myocardium. METHODS Twenty-four SD rats were divided randomly into three groups: the control group, the high temperature and high humidity stress group, and the heat stress group. All examinations were performed four weeks later. Mean arterial blood pressure (MBP) was measured by carotid artery intubation and reactive oxygen species (ROS) was determined with spectrophotometer. The concentration of AngⅡ in the plasma and myocardium was detected respectively by radioimmunoassay and expression level of p22phox mRNA in myocardium was determined by reverse transcription polymerase chain reaction (RT-PCR). P22phox protein was detected by immunohistochemistry and semi-quantitative analysis in different groups. RESULTS Four weeks after heat stress, MBP in the heat stress group and the high temperature and high humidity stress group increased significantly (P<0.01), but no significant difference was observed in LVW/BW index (P>0.05) compared with those in the control group. The concentration of AngⅡ in the plasma and the myocardium and the ROS level of myocardium significantly increased (both P<0.01), and the expression of p22phox mRNA and protein levels of myocardium also increased significantly (P<0.01) in the heat stress group and the high temperature and high humidity stress group. CONCLUSION The concentration of AngⅡ in the plasma and myocardium and p22phox in the myocardium increase in heat stress conditions. Heat stress may be associated with over production of ROS, which is induced by increased expression of AngⅡ.
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