Endometritis is the most common pathology in animals. However, in the context of an inflamed endometrium, alterations occur in the production of prostaglandins (PG s) and the noradrenergic innervation of the uterus, although the precise relationship between noradrenaline (NA), adrenoreceptors (AR s), and the output of PG F2α remains unclear. To clarify this issue, the participation of α1-, α2- and β-AR s in NA-influenced PG F synthase (PG FS) and PG 9-ketoreductase/carbonyl reductase (CBR1) protein abundances in the porcine inflamed endometrium, and the secretion of PG F2α from the tissue were determined. E. coli suspension (E. coli group) or saline (CO N group) was injected into the uterine horns. After eight days, severe acute endometritis was diagnosed in the E. coli group. Endometrial explants were treated with NA and/or α1-, α2- and β-AR s antagonists. In the CO N and E. coli groups, NA increased endometrial PG FS and CBR1 protein abundances and PG F2α secretion, compared to the control values (obtained from an endometrium that had not undergone any in vitro treatment). In the E. coli group, NA-stimulated CBR1 protein abundance and PG F2α release were higher, while PG FS protein abundance was lower than in the CO N group. In the latter group, the antagonists of α1A-, α1D-, α2B- and α2C-AR s isoforms and β2- AR s subtype decreased NA-stimulated PG FS protein abundances, compared to NA action alone. In the E. coli group, this effect on PG FS abundances evoked α1D-, α2C-, β1- and β2-AR s antagonists with NA. Antagonists of α1B-, α2B-, β1- and β2-AR s in the CO N group and antagonists of α1B-, α1D-, α2A-, α2C-, β1- and β2-AR s in the E. coli group eliminated a rise in the NA-stimulated CBR1 abundance of protein versus the NA influence alone. In comparison to NA effect alone, α1D-, α2C- and β2-AR s antagonists with NA reduced PG F2α secretion in both the CON and E. coli groups. Such effect on PG F2α release was also exerted in the E. coli group by α1B-, α2A- and β1-AR s antagonists with NA. Summarizing, in the porcine inflamed endometrium, NA increases PG FS protein abundance via α1D-, α2C- and β(1, 2)-AR s, and CBR1 protein abundance and PG F2α release by α1(B, D)-, α2(A, C) and β(1, 2)-AR s. The obtained findings suggest that, in an indirect manner, NA may affect the PG F2α-regulated processes by influencing its production and secretion. The results could offer new targets for drugs to regulate inflammation and improve uterine and ovarian functions.
