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 β3‐AR in left ventricle of rats exposed to acute (1 day) and long‐term (28 days) cold, but no changes in β1‐ and β2‐AR mRNA levels. However, single immobilization significantly decreased β2‐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 β2‐AR mRNA levels as seen in intact animals. Moreover, β1‐ and β2‐AR did not show any significant changes. Surprisingly, the most prominent changes in the heart were detected for α1B‐AR gene expression. We found decreased levels of α1B‐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 α1B‐AR mRNA levels in heart. It seems that while β‐AR undergoes adaptation, α1B‐AR is probably prepared to modulate heart functions. Proposed mechanism of β‐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 β2‐, β3‐AR, and α1B‐AR in the process of heart adaptation to chronic stress exposure is proposed.