Pharmacological studies using the Doppler technique revealed that pregnancy
decreases the systemic blood pressure and enhances uterine blood velocity
in rats. The reactivity of the uterine artery to alpha -adrenoceptor and mu
scarinic receptor agonists was higher than that of systemic arteries. Sodiu
m nitroprusside increased uterine arterial blood velocity slightly during g
estation and markedly in non-pregnant rats. N-G-L-Arginine methyl ester (L-
NAME) decreased the uterine blood velocity mainly in gravid animals. The ef
fect of diclofenac on uterine blood velocity was also more pronounced durin
g pregnancy. The actions of sodium nitroprusside, L-NAME and diclofenac on
systemic blood pressure were similar in pregnant and virgin rats. Altogethe
r, these results indicate that pregnancy enhances nitric oxide (NO) and vas
odilatory prostanoid production in the uterine vascular muscle which become
s less sensitive to exogenous NO. The uterine vasodilated status appears to
be determined by conjugated actions of endothelial NO and vasodilator pros
tanoids of which the synthesis and the effects are weakly modified in syste
mic arteries during gestation. (C) 2001 Elsevier Science B.V. All rights re
served.