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Acta Physiologica 2007; Volume 191, Supplement 658
Joint Meeting of The Slovak Physiological Society, The Physiological Society and The Federation of European Physiological Societies
9/11/2007-9/14/2007
Bratislava, Slovakia
STRESS INDUCED CHANGES IN THE GENE EXPRESSION OF ADRENOCEPTORS IN RAT HEART
Abstract number: PF17-139
Tillinger1 A., Myslivecek2 J., Petrak1 J., Krizanova3 O., Kvetnansky1 R.
1Institute of Experimental Endocrinology, Slovak Academy of Sciences, Bratislava, Slovakia
2First Faculty of Medicine, Charles University, Prague, Czech Republic
3Institute of Molecular Physiology and Genetics, Slovak Academy of Sciences, Bratislava, [email protected]
Aims:
Stress-induced elevation of plasma noradrenaline and adrenaline levels is well established response of the organism, which should stimulate adrenoceptors (AR) and lead to changes in mRNA and protein levels in the heart. The aim of this study was to measure mRNA levels of AR in heart atria and ventricles during exposure to immobilization (IMO) or cold stress.
Methods:
Changes in gene expression of AR were studied by RT PCR in animals exposed to acute and repeated/chronic IMO and cold.
Results:
Nosignificant changes in mRNA levels of b1-AR in the hearts of rats exposed toIMO or cold were found. On the other hand a significant decrease in b2-AR mRNA levels in atria and ventricles of immobilized animals were shown. Inhearts of cold stressed animals no changes of the b2-AR at mRNA levels weredetected. Unexpectedly, we found a significant increase of b3-AR mRNA levels in atria and ventricles of IMO rats. Increase in b-AR mRNA levels was 3 also observed in ventricle of cold stressed animals. No significant changes of a1B-AR mRNA levels were observed in hearts of animals exposed to IMO. In cold stressed animals we found a significant decrease of a1B-AR mRNA levels in atria and ventricles.
Conclusion:
Our results point to different regulation of individual types of AR by various stressors. Also, since b2-, b3-AR and a1B-AR are expressed in the opposite manner, their role in the process of heart adaptation to stress is likely possible. Nevertheless, further experiments must verify this proposal.
This work was supported by: APVV grant 0148-06 and VEGA grant 2/5125.
To cite this abstract, please use the following information:
Acta Physiologica 2007; Volume 191, Supplement 658 :PF17-139