Effect of estrogen on muscarinic acetylcholine receptor expression in rat myometrium

Abdalla, Fernando Maurício Francis; Maróstica, Elisabeth; Picarelli, Zuleika P.; Abreu, Lygia C.; Avellar, Maria Christina W.; Porto, Catarina S.

doi:10.1016/j.mce.2003.10.040

Cited by 30 publications

(21 citation statements)

References 43 publications

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“…following oestrogen impregnation. Furthermore, it was observed that administration of oestradiol to non-pregnant rats resulted in a sharp decrease in the EC 50 value for CCh-induced uterine contraction (Abdalla et al 2004), similar to that observed in our study between pregnancy and term. Because an abrupt increase in plasma and myometrial oestrogen occurred at the onset of parturition, we suggest that the mR signalling pathway is influenced by changes in the hormonal status between day 15 of pregnancy and term.…”

Section: Discussionsupporting

confidence: 90%

“…In contrast to the PLC-coupled receptors described above, no detectable changes in the density and properties of the M 3 receptor were observed during the course of pregnancy (Lajat et al 1996). In correlation with these data, oestradiol treatment did not affect the expression of M 3 receptor in rat myometrial cells (Abdalla et al 2004). However, we have previously shown that the expression of Gq , the transducer protein that links mR and OTR to PLC , increases at the end of pregnancy (CohenTannoudji et al 1995).…”

Section: Introductionsupporting

confidence: 56%

“…Indeed, while OTR is downregulated by progesterone during pregnancy and upregulated by oestradiol near term (Larcher et al 1995), the density of rat myometrial M 3 subtype remains unchanged throughout pregnancy (Lajat et al 1996). Furthermore, neither ovariectomy nor oestradiol treatment affected the density of rat myometrial M 3 subtype (Choppin et al 1999, Abdalla et al 2004. The increased potency of CCh to induce InsP production and uterine contraction at term is therefore probably related to changes occurring downstream of the M 3 receptor, at the level of G protein and/ or PLC enzymes.…”

Section: Discussionmentioning

confidence: 99%

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Up-regulation of rat myometrial phospholipases Cβ1 and Cβ3 correlates with increased term sensitivity to carbachol and oxytocin

Houdeau

Levy²,

Mhaouty-Kodja³

2005

Journal of Endocrinology

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In the present study, we compared rat uterine contractility and myometrial inositol phosphate (InsP) production in response to activation of muscarinic and oxytocin receptors during pregnancy and at term. The level of myometrial phospholipase (PL) C was also determined by Western blotting at different stages of pregnancy and following administration of oestradiol, progesterone or vehicle. The results showed an increased potency of carbachol (CCh), a cholinergic muscarinic agonist, and oxytocin (OT) to enhance myometrial InsP production at term. This correlated with an increased potency of both agonists to induce contraction of the circular but not the longitudinal muscle. For both InsP production and contractile activity, the maximal response of CCh was unaltered, while that of OT was significantly increased. Interestingly, the increased responsiveness to CCh and OT was associated with an up-regulation of PLC 1 and PLC 3 enzymes. Such regulation is under the control of oestradiol since administration of this steroid to pregnant rats increased the amount of both enzymes by 200-260%. In contrast, progesterone administration was without effect. The present study presents the first evidence that the expression of rat myometrial PLC 1 and PLC 3 is under the positive control of oestradiol. This could participate in the enhancement of myometrial InsP accumulation and uterine contraction at term in response to CCh and OT. Based on contraction studies, we also propose that the longitudinal and circular uterine muscles differ in the regulation of the PLC pathway during pregnancy.

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Section: Discussionsupporting

confidence: 90%

Section: Introductionsupporting

confidence: 56%

Section: Discussionmentioning

confidence: 99%

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Up-regulation of rat myometrial phospholipases Cβ1 and Cβ3 correlates with increased term sensitivity to carbachol and oxytocin

Houdeau

Levy²,

Mhaouty-Kodja³

2005

Journal of Endocrinology

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“…A previous study indicated that EDHF-mediated mesenteric vasodilation in response to nonreceptor stimulation with the Ca 2ϩ ionophore A-23187 is potentiated by estrogen (32). Also, estrogen replacement produced no change in the expression of muscarinic receptors in the rat uterus (1). Together, these data suggest that it is unlikely that estrogenic enhancement of ACh-evoked responses is induced by increased expression of endothelial muscarinic receptors.…”

Section: Discussionmentioning

confidence: 64%

Estrogen replacement enhances EDHF-mediated vasodilation of mesenteric and uterine resistance arteries: role of endothelial cell Ca²⁺

Burger

Kuzina

Osol

et al. 2009

American Journal of Physiology-Endocrinology and Metabolism

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Burger NZ, Kuzina OY, Osol G, Gokina NI. Estrogen replacement enhances EDHF-mediated vasodilation of mesenteric and uterine resistance arteries: role of endothelial cell Ca 2ϩ . Am J Physiol Endocrinol Metab 296: E503-E512, 2009. First published January 6, 2009 doi:10.1152/ajpendo.90517.2008.-Endothelium-derived hyperpolarizing factor (EDHF) plays an important role in the regulation of vascular microcirculatory tone. This study explores the role of estrogen in controlling EDHF-mediated vasodilation of uterine resistance arteries of the rat and also analyzes the contribution of endothelial cell (EC) Ca 2ϩ signaling to this process. A parallel study was also performed with mesenteric arteries to provide comparison with a nonreproductive vasculature. Mature female rats underwent ovariectomy, with one half receiving 17␤-estradiol replacement (OVXϩE) and the other half serving as estrogen-deficient controls (OVX). Uterine or mesenteric resistance arteries were harvested, cannulated, and pressurized. Nitric oxide and prostacyclin production were inhibited with 200 M N G -nitro-L-arginine and 10 M indomethacin, respectively. ACh effectively dilated the arteries preconstricted with phenylephrine but failed to induce dilation of vessels preconstricted with high-K ϩ solution. ACh EC50 values were decreased by estrogen replacement by five-and twofold in uterine and mesenteric arteries, respectively. As evidenced by fura-2-based measurements of EC cytoplasmic Ca 2ϩ concentration ([Ca 2ϩ ]i), estrogen replacement was associated with increased basal and ACh-stimulated EC [Ca 2ϩ ]i rise in uterine, but not mesenteric, vessels. These data demonstrate that EDHF contributes to endothelium-dependent vasodilation of uterine and mesenteric resistance arteries and that estrogen controls EDHFrelated mechanism(s) more efficiently in reproductive vs. nonreproductive vessels. Enhanced endothelial Ca 2ϩ signaling may be an important underlying mechanism in estrogenic modulation of EDHFmediated vasodilation in small resistance uterine arteries. endothelium-derived hyperpolarizing factor; acetylcholine; fura-2; high potassium THE VASCULAR ENDOTHELIUM plays an important role in the control of blood vessel tone through release of relaxing and contracting factors in response to mechanical or agonist-

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“…Uterine activity is regulated by complex and mutual interactions among sex steroids, neurohypophysial hormones, and neurotransmitters (4). It also involves the integration of many signal-transducing events, resulting in precise coordination of myometrial contractile activity.…”

mentioning

confidence: 99%

Differences in muscarinic-receptor agonist–, oxytocin-, and prostaglandin-induced uterine contractions

Dittrich

Mueller

Oppelt

et al. 2009

Fertility and Sterility

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Effect of estrogen on muscarinic acetylcholine receptor expression in rat myometrium

Cited by 30 publications

References 43 publications

Up-regulation of rat myometrial phospholipases Cβ1 and Cβ3 correlates with increased term sensitivity to carbachol and oxytocin

Up-regulation of rat myometrial phospholipases Cβ1 and Cβ3 correlates with increased term sensitivity to carbachol and oxytocin

Estrogen replacement enhances EDHF-mediated vasodilation of mesenteric and uterine resistance arteries: role of endothelial cell Ca²⁺

Differences in muscarinic-receptor agonist–, oxytocin-, and prostaglandin-induced uterine contractions

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Effect of estrogen on muscarinic acetylcholine receptor expression in rat myometrium

Cited by 30 publications

References 43 publications

Up-regulation of rat myometrial phospholipases Cβ1 and Cβ3 correlates with increased term sensitivity to carbachol and oxytocin

Up-regulation of rat myometrial phospholipases Cβ1 and Cβ3 correlates with increased term sensitivity to carbachol and oxytocin

Estrogen replacement enhances EDHF-mediated vasodilation of mesenteric and uterine resistance arteries: role of endothelial cell Ca2+

Differences in muscarinic-receptor agonist–, oxytocin-, and prostaglandin-induced uterine contractions

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Estrogen replacement enhances EDHF-mediated vasodilation of mesenteric and uterine resistance arteries: role of endothelial cell Ca²⁺