Immunohistochemical reactivity of myometrial oxytocin receptor in extracorporeally perfused nonpregnant human uteri

Abstract

Taken together, our data demonstrate that the dynamics of oxytocin receptor expression can be affected by stimulation with 17-beta-estradiol and oxytocin not only in the pregnant uterus, but also in the nonpregnant uterus. Therefore, dyscontractile phenomena of the nonpregnant myometrium also may be mediated via 17-beta-estradiol, oxytocin and the oxytocin receptor.

Perfused Non-Pregnant Swine Uteri: A Model for Evaluating Transport Mechanisms to the Side Bearing the Dominant Follicle in Humans

“…Previous investigations validated the feasibility of this perfusion model of isolated uteri for various purposes [11,12,[18][19][20][21][22][23]. According to previously reported in vitro experiments, there is a possible clinical relationship between uterine contractility and steroid hormones [24,25].…”

“…Furthermore, the receptorm e d i a t e d r e a c t i v i t y o f t h e n o n -p r e g n a n t myometrium is modulated in a characteristic way by treatment with 17β-estradiol, oxytocin, or a combination of the two [23]. Stimulation with highdose of 17β-estradiol increased myometrial OTR density, with maximum levels found in the uterine fundus [11]. In particular, pretreatment with 17β-estradiol before oxytocin stimulation resulted in a larger and more prolonged uterine response to oxytocin application [23], while progesterone stimulation directly resulted in a reduction of both the frequency and duration of uterine contractility, as reported by Bulletti et al [21].…”

“…17β-estradiol stimulation increased both the frequency and duration of rhythmical electrical activity, as well as endoluminal pressure, in five extracorporeal perfused human uteri [21]. Richter et al [11] reported that OTR expression is up-regulated by 17β-estradiol and oxytocin in nonpregnant uteri. Furthermore, the receptorm e d i a t e d r e a c t i v i t y o f t h e n o n -p r e g n a n t myometrium is modulated in a characteristic way by treatment with 17β-estradiol, oxytocin, or a combination of the two [23].…”

“…It has been shown in rodents that oxytocin, a potent uterotonic agent, and its receptor (OTR) mRNA expression are at their highest levels at estrus and are up-regulated by estrogens [10]. Furthermore, Richter et al [11] reported that OTR expression is also up-regulated by estrogens in humans, especially in the fundus of the uterus, not only in pregnant uteri but also in non-pregnant uteri [11,12]. It has therefore been b e l i e v e d t h a t e s t r o g e ns s t i m u l a t e u t e r i n e contractility via OTR up-regulation, and uterine contractility or uterine contraction waves has been believed to be responsible for the mechanisms of rapid sperm transport [3][4][5].…”

In Vitro Contractile Response of Rabbit Myometrium to BKCa and KATP Potassium Channel Openers

“…Both ER and PR are members of the steroid receptor superfamily that act though the steroid-modulated transcription factors (Kurita et al 2000). The oestrogenic state of the pregnant as well as non-pregnant uterus (Richter et al 2003) is linked to the elevation of myometrial smooth muscle reactivity: increased expression of oxytocin (OXY) receptors and a blockade of the potassium current (Knock et al 2001). Progesterone is responsible for uterine quiescence, hence in relation to uterine contractility it produces the opposite activity to oestrogen by decreasing the number of OXY receptors and increasing the potassium current (Knock et al 2001).…”