Tyrosine hydroxylase (TH) is the rate-limiting enzyme of the synthesis of catecholamines (CA) in the catecholaminergic neurons and neuropeptide Y (NPY) is a cotransmitter of CA. Chronic stress leads to increased levels of plasma CA together with increased levels of TH and its gene expression in the adrenal medulla. Here, we investigated TH and preproNPY mRNA expressions in the hearts of two rat strains submitted to various stress protocols by real-time RT-PCR method. A restraint stressor (immobilization, IMO) and restraint stressor combined with partial immersion of rats into water (IMO+C) were applied for 1 hour to adult Lewis (Lew) rat, which shows a blunted hypothalamic-pituitary-adrenal (HPA) response, and to an comparator strain, Sprague Dawley (SD) rat. TH and preproNPY mRNA expressions were determined in four groups of animals after 1 and 3 hours after IMO and IMO+C (IMO1, IMO3, IMO+C1, IMO+C3) and compared to control animals. TH mRNA expression in the right atria of SD rats increased significantly (by 365% and 239%) after IMO3 and IMO+C3, respectively. An increase by 80% was also observed in the left atria after IMO+C3. In Lew rats, an increase by 73% was observed only in the left atria after IMO3. In SD rats, a significant decrease of preproNPY mRNA expression after IMO1 and IMO+C1 by 54% and 46%, respectively was observed in the right ventricles. A decline by 38% was also found in the left ventricle after IMO1. In Lew rats, preproNPY mRNA expressions have shown a decline in the right atria by 52% after IMO3 and by 58% in the left ventricles after IMO+C3. In conclusion, differential effects were observed between mRNA expressions for TH and preproNPY in all heart compartments in various stress protocols, however, a tendency for an increase in TH mRNA and a decline in preproNPY mRNA expressions were seen in both strains of animals. Our data show that increased TH mRNA expression in the heart in acute stress which may reflect increased synthesis of CA is not associated with increased expression of its main cotransmitter, NPY.

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