Objective: 

Mammalian cardiomyocytes produce atrial natriuretic peptide (ANP) with regulatory role in body fluid homeostasis. ANP induces suppression of the renin-angiotensin as well as the sympathetic nervous systems to protect cardiovascular homeostasis, which is also deteriorated by the stress. Here, we investigated whether ANP mRNA expression in the heart could be affected by stress.

Methods: 

Heart preparations were analyzed by real-time RT-PCR. The two rat strains, Sprague-Dawley (SD) and Lewis (LEW), were used, the latter being known to have a blunted hypothalamic-pituitary-adrenal response. A restraint stressor (immobilization, IMO) and IMO combined with partial immersion of rats into water (IMO+C) were applied to rats for one hour. One or three hours after the stress termination, the rats were decapitated, hearts removed, and each atrium and ventricle were examined separately. Expressions of ANP mRNA were determined in controls and stressed rats (IMO1, IMO3, IMO+C1, IMO+C3).

Results: 

Expression of ANP mRNA in the right atria of SD rats increased significantly by 47% after IMO1. An increase by 41% after IMO3 was observed in the left atria. IMO1, IMO3, and IMO1+C3 caused a significant increase of the ANP mRNA expression also in the left ventricles. However, a decline by 27% and 29% was shown after IMO1 and IMO+C1, respectively, in the right atria of LEW rats.

Conclusions: 

Restraint stressors induced changes in expression of ANP mRNA in cardiomycytes of atria and left ventricles; these effects may have relevance to ANP-induced cardioprotection.

Supported by grants MSM0021620806 and MSM0021620819.