Prevention of estrogen-induced uterine hyperemia by alpha-adrenergic receptor-blocking agents.
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Biomedical subjects
Publications and source records attributed to K E Clark.
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Earlier studies from these laboratories have demonstrated that prostaglandins (PG's) of the A and E series are potent uterine vasodilators whereas PGF's do not significantly alter uterine vascular resistance. In addition, PGE's and PGF's are also able to modify adrenergic vasoconstrictor responses in the canine uterus. In the present study the role of endogenous prostaglandins in regulating uterine vascular resistance and adrenergic neurotransmission was evaluated. Intra-arterial infusion of the prostaglandin synthesis inhibitor meclofenamate resulted in a significant reduction in PGE levels in uterine venous plasma and increased vascular resistance. Uterine vasoconstrictor responses produced by sympathetic nerve stimulation and norepinephrine were enhanced when endogenous PG synthesis was inhibited. During sympathetic nerve stimulation, uterine venous plasma levels of radioimmunoassayable prostaglandins of the E of F series did not change, suggesting that the adrenergic activation of PG synthesis is not detectable in uterine venous efferent. These data suggest that endogenous prostaglandins of the E series appear to play an important role in regulating uterine blood flow (I) by relaxing uterine vascular smooth muscle and (2) by depressing adrenergic vasoconstrictor responses.
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Prostaglandins appear to play an important role in a number of reproductive processes. The present study was designed to determine if the vasodilator action of prostaglandins of the A and E series on uterine vascular smooth muscle was mediated via a receptor and if PGF2alpha could compete for this same receptor. The data demonstrate that PGF2alpha, which by itself has no uterine vascular effect, can produce a parallel shift in the dose-response curves for certain vasodilator prostaglandins. This action, which suggests competitive antagonism, may well play a role in regulating blood flow in the nonpregnant uterus.
Prostaglandins appear to play an important role in a number of reproductive processes. The effect of prostaglandins on numerous vascular beds has been extensively studied, but the effects on uterine hemodynamics have not. The present study was designed to determine the effects of prostaglandins of the A and E series on uterine vascular resistance and responses to adrenergic nerve stimulation in the canine uterus. PGE1, PGE2 and PGA1 were found to be potent uterine vasodilators. In addition, these agents were able to modify adrenergic vasoconstrictor responses. These effects on uterine vascular resistance and adrenergic vasoconstrictor responses were separable. The results of these studies suggest that prostaglandins of the A and E series may play an important role in regulating uterine blood flow in the nonpregnant animal.