Objective: 

Alteration of cardiovascular activity caused by stress is induced by activation of sympathetic nervous system (NS). Whether parasympathetic NS participates on stress-induced responses has not been extensively studied. Principal neurotransmitter of parasympathetic NS is acetylcholine, which exerts its function by activation of muscarinic receptors.

Methods: 

In the rat heart atria we studied the expression of mRNAs for muscarinic M2 receptors (M2R) and for choline acetyltransferase (CHAT), enzyme forming acetylcholine. We used two rat strains, Sprague-Dawley (SD) and Lewis (LEW), 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. Rats were killed three hours after stress termination. Relative expression of mRNA for both genes, estimated with Real-Time PCR, was expressed as a ratio of target gene Cq value to Cq value of reference gene.

Results: 

IMO+C caused increased expression of mRNA for CHAT; this effect was more pronounced in SD than in LEW rats. Expression of mRNA for M2 receptors was decreased by IMO in both rat strains. Exposure to two types of restraint stressors caused similar changes in CHAT and M2R mRNA production in the heart atria of both SD and LEW rats.

Conclusions: 

In the heart atria we demonstrated the expression of mRNA both for enzyme forming acetylcholine and its M2 receptor. Present studies did not show the differences in response to two restraint stressors.

Supported by grants MSM 0021620806 and MSM 0021620819.