Effect of prostaglandins (F2 alpha, E1, and E2) on blood pressure and oxytocin-induced intramammary pressure responses in rats.

In lactating rats, vasoactive prostaglandin (PG) doses of F2 alpha (4 and 8 microgram/kg), E1, and E2 (2 and 4 microgram/kg each) reduced the intramammary pressure response to standard iv doses of 300 microU oxytocin by 50--80%. Adrenergic blockers, phenoxybenzamine and/or propranolol (1 mg/kg each sc) did not influence the blood pressure response to PGF2 alpha, PGE1, or PGE2. The oxytocin-antagonistic action of a single iv PGF2 alpha dose (4 microgram/kg) could not be altered by adrenergic blockers. In contrast, the oxytocin-antagonistic effects of PGE1 and PGE2 (2 microgram/kg each) were completely eliminated after alpha-receptor blockade, while the activity of oxytocin was augmented. Under beta-receptor or alpha- and beta-receptor blockade, the oxytocin-antagonistic effects of PGE1 and PGE2 were almost abolished. alpha-Receptor blockade reduced the oxytocin-antagonistic action of infused PGF2 alpha (8 microgram/kg.min for 15 min) by 38%. beta- or alpha- and beta-receptor blockade had no effect. The oxytocin-antagonistic actions of PGE1 and PGE2 (4 microgram/kg.min for 15 min each) were greatly reduced under alpha-receptor blockade. beta-Receptor blockade had no influence on the oxytocin-antagonistic activities of PGE1 or PGE2; under alpha- and beta-receptor blockade, the inhibitory actions of PGE1 and PGE2 were reduced by 60--70%. Mechanisms of PG-induced inhibition of the oxytocin response may involve mammary vasoconstriction and/or alterations in myoepithelial activity of cAMP and cGMP.