Effect of pregnancy on the roles of nitric oxide and prostaglandins in 5-hydroxytryptamine-induced contractions in rat isolated thoracic and abdominal aorta.

1. Vascular resistance and sensitivity to circulating pressor and vasoconstrictor substances are blunted during pregnancy. This has been attributed mainly to an increased production of endothelium-derived mediators. The aim of the present study was to determine whether pregnancy changes the relative participation of nitric oxide (NO) and prostaglandins (PG) in the modulation of the contractile response to 5-hydroxytryptamine (5-HT) in two anatomically distint segments of the rat aorta. 2. Full concentration-response curves to 5-HT were obtained in isolated rings from the thoracic and abdominal portion of the aorta from pregnant and non-pregnant rats in the presence and absence of the NO synthase (NOS) inhibitor N(G)-nitro-l-arginine methyl ester (L-NAME; 10 micromol/L) or the PG synthesis inhibitor indomethacin (10 micromol/L). Cyclo-oxygenase (COX)-1, COX-2 and endothelial (e) NOS protein expression were determined in the same tissues by immunoblot. 3. The effects of pregnancy were accentuated in the abdominal compared with the thoracic aorta. In addition, the relative participation of the NO and PG pathways seems to be changed during pregnancy. Although NO seems to be the mediator mainly responsible for the effect of pregnancy in the thoracic aorta, our results suggest a complex interaction between NO and PG in the abdominal aorta. Indomethacin significantly reduced the contractile response of both segments of the aorta, whereas expression of COX-1, COX-2 and eNOS were increased only in the abdominal segment of pregnant animals. 4. These results show that the effect of pregnancy is not homogeneous along the aorta. There seems to be a mutual interaction between PG and NO in the abdominal, but not in the thoracic, aorta from pregnant rats: the role of NO becomes evident in the absence of vasodilatory PG, whereas the participation of the latter increases in the absence of NO working as a compensatory mechanism.