Gene Expression of Adrenoceptors in the Hearts of Cold-Acclimated Rats Exposed to a Novel Stressor

Changes in the heart rate and force of contraction are regulated by catecholamines via adrenoceptors (AR). In this work, we measured gene expression of AR in left heart atria and ventricles in rats exposed to cold stress and in cold-acclimated rats exposed to a novel stressor (immobilization). We found a significant increase in beta(3)-AR in left ventricle of rats exposed to acute (1 day) and long-term (28 days) cold, but no changes in beta(1)- and beta(2)-AR mRNA levels. However, single immobilization significantly decreased beta(2)-AR mRNA levels both in left atria and ventricles compared to acute cold stress. Application of a novel stressor (immobilization) to previously cold-acclimated animals did not show decrease of beta(2)-AR mRNA levels as seen in intact animals. Moreover, beta(1)- and beta(2)-AR did not show any significant changes. Surprisingly, the most prominent changes in the heart were detected for alpha(1B)-AR gene expression. We found decreased levels of alpha(1B)-AR mRNA in the heart of rats exposed to cold and immobilization. We also found that exposure of cold-acclimated rats to immobilization is responsible for additional decrease of alpha(1B)-AR mRNA levels in heart. It seems that while beta-AR undergoes adaptation, alpha(1B)-AR is probably prepared to modulate heart functions. Proposed mechanism of beta-AR adaptation needs to be elucidated. Thus, we have shown that gene expression of different AR subtypes in the heart is regulated differently by various stressors. A protective role of beta(2)-, beta(3)-AR, and alpha(1B)-AR in the process of heart adaptation to chronic stress exposure is proposed.