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Phenylethanolamine N ‐Methyltransferase Gene Expression in the Heart and Blood Pressure Response to Oxytocin Treatment in Rats Exposed to Voluntary Wheel Running
Author(s) -
Bakos Jan,
Bobryshev Peter,
Tillinger Andrej,
Kvetňanský Richard,
Jezova Daniela
Publication year - 2008
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1196/annals.1410.031
Subject(s) - oxytocin , phenylethanolamine , medicine , endocrinology , blood pressure , wheel running , turnover , methyltransferase , gene expression , chemistry , gene , immunohistochemistry , biochemistry , management , tyrosine hydroxylase , methylation , economics
This study aimed to contribute to the knowledge of cardiovascular regulation associated with repeated exercise by evaluating untraditional parameters in the model of voluntary wheel running. Possible changes in cardiac phenylethanolamine N ‐methyltransferase (PNMT) gene expression were evaluated using running for 3 weeks in four rat strains, and the hypothesis that voluntary wheel running modifies mean arterial pressure (MAP) responses to oxytocin administration was verified. Running activity increased gradually and was high in spontaneously hypertensive rats (SHR) and Sprague‐Dawley rats, while low in Wistar rats. The levels of PNMT mRNA in the left but not right atrium increased significantly in rat strains exhibiting high physical activity. Concentrations of PNMT mRNA were significantly higher in SHR and Sprague‐Dawley compared to those in Wistar rats, which ran much shorter distances. MAP was found to be higher in rats exposed to voluntary running, which might be the result of the cessation of the exercise 24 h before the measurements. Oxytocin treatment (5 μg/kg and 30 μg/kg i.v.) resulted in significant increase in MAP in both control and running animals in a dose‐dependent manner. In conclusion, voluntary wheel running failed to modify sensitivity to cardiovascular action of oxytocin but resulted in increased gene expression of PNMT in left, but not right, heart atrium in a running activity–dependent manner.