Role of Estradiol-17beta and Progesterone in Regulating Constriction of Ovine Uterine Arteries

Abstract

The role of estradiol-17.beta. (E2) and progesterone (P4) in regulating the constriction of uterine arteries was investigated. Segments of uterine arteries from ovariectomized control and steroid-treated (E2, P4 and E2 + P4) ewes were perfused with agents which enhance (prostaglandin F2.alpha. and norepinephrine) or suppress (phentolamine; blocker of .alpha.-adrenergic receptors) vasoconstriction provoked by periarterial adrenergic nerve stimulation (NS). Treatment of ewes with P4 increased (P < 0.01) while treatment with E2 decreased (P < 0.01) vasoconstriction to NS following perfusions of saline (control vehicle), prostaglandin F2.alpha. (PGF2.alpha.) or norepinephrine (NE) compared to evoked responses of arteries from control or E2 + P4-treated ewes. Arteries from control and E2 + P4-treated ewes did not differ in their response to NS after perfusion of any drug or the vehicle. Regardless of steroid effects, vasoconstriction to NS was markedly enhanced by NE (P < 0.01) but was not affected by PGF2.alpha.. Steroid treatment did not affect the response of arteries to phentolamine which blocked vasoconstriction to NS (P < 0.01). Ability of phentolamine to block vasoconstriction indicated that .alpha.-adrenergic receptors mediated the stimulatory effects of the neurotransmitter. Displacement of phentolamine by repeated perfusions of excess NE resulted in an increase in constriction to NS by arteries from all ewes except those treated with estradiol only (P < 0.01). These data suggest that estrogen and progesterone regulate uterine vasoconstriction by altering the function of periarterial sympathetic nerves and/or the .alpha.-adrenergic receptors.