Hormonal influence on ionic channels in myometrium

Ludmir, Jack; Erulkar, S. D.

doi:10.1002/jemt.1070250206

Cited by 10 publications

(3 citation statements)

References 42 publications

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“…The data showed an inhibitory effect of oestradiol, inward Ca 2+ current was decreased and there was a leftward shift of around 7 mV in the inactivation curve for the channels. These data fit with those obtained by Ludmir & Erulkar (71) in 1973, who reviewed the available data on hormonal effects on myometrial ion channels of rat and human myometrium. Together, these results suggest that acting acutely oestrogens will be inhibitory on the myometrium, suppressing the generation of action potentials.…”

Section: Sex Hormones and Calcium Currentsupporting

confidence: 87%

Sex Hormones and Excitation–Contraction Coupling in the Uterus: The Effects of Oestrous and Hormones

Wray

Noble

2008

J Neuroendocrinology

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The purpose of this review is to evaluate what is known and not known about the effects of oestrous and its hormones on uterine contractility and excitability, and to assess how important, hormonal differences in nonpregnant animals are to Ca 2+ signalling mechanisms. Although the physical effects of oestrous on the uterus and the underlying hormonal changes have been known for many decades, there have been few attempts to integrate this knowledge with the molecular and cellular information more recently gathered on the mechanisms of excitation-contraction (EC) coupling. Many reports have advanced our understanding of differences in EC coupling between pregnant and nonpregnant uterus, but few have specified the hormonal status of the nonpregnant animal. Does this have consequences for the conclusions drawn? In this brief review, we firstly overview EC-coupling and then describe the oestrous cycle and its effects on mechanical activity. We then look in detail at the effects of hormonal changes on Ca 2+ entry and excitability in uterine cells, effects on internal Ca 2+ release from the sarcoplasmic reticulum (SR) and then review information about electrical activity at different stages of oestrous. We then examine recent evidence that effects of hormonal changes may be mediated through membrane lipid rafts and caveolae. We present our findings on myometrial Ca 2+ signalling at different stages of oestrous and use them as a focus to summarise the main findings of this review. We hope that this will be a stimulant to our colleagues studying myometrial physiology and pathophysiology; to deepen understanding and increase appreciation of the possible effects of oestrous and sex hormones on their studies.Excitation-contraction coupling in the uterus: an overview Several reviews on this topic have recently been published and should be consulted for details and additional references (1-8 Journal of NeuroendocrinologyCorrespondence to: Susan Wray, Department of Physiology, The University of Liverpool, Liverpool L69 3BX, UK (e-mail: s.wray@liv.ac.uk).In this review, we examine how far the increased understanding that we have of the events in excitation contraction can explain the effects of the oestrous cycle and sex hormones on uterine function. Observational studies of electrical and mechanical activity in the rat myometrium have shown a relative quiescence during pro-oestrous, with little propagation of any electrical events. Thus, uterine activity can be said to approximately inversely reflect plasma 17b-oestradiol concentrations. We show that Ca 2+ signalling and mechanical activity are greatest in metoestrous and dioestrous compared to pro-oestrous and oestrous. These data are discussed in terms of hormonal effects on Ca 2+ and K + channels. Finally, the influence of sex hormones on lipid rafts and caveolae are considered and discussed in relation to recent findings on their role in uterine signalling and contractility, and cholesterol levels and obesity.

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Section: Sex Hormones and Calcium Currentsupporting

confidence: 87%

Sex Hormones and Excitation–Contraction Coupling in the Uterus: The Effects of Oestrous and Hormones

Wray

Noble

2008

J Neuroendocrinology

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“…Alternative pathways in which progesterone may exert an effect could be via sodium or chloride channels. There is some evidence to suggest that sodium channels may be upregulated in myometrium at late gestation 20 but the distinct roles of specific sodium channels is not clearly understood. Ion channels may well have regulatory pathways related to myometrial function but whether progesterone uses them in its mechanism to prevent preterm labor remains unclear.…”

Section: Discussionmentioning

confidence: 99%

The Effect of Progesterone on Myometrial Contractility, Potassium Channels, and Tocolytic Efficacy

et al. 2009

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“…Uterine smooth muscle cells contain a diversity of ion channels that regulate membrane excitability (1)(2)(3). The large-conductance Ca 2+ -activated K + channel (maxi-K) has been shown to play a significant role in modulating uterine function (4)(5)(6).…”

Section: Introductionmentioning

confidence: 99%

Regulation of the Ca2+-sensitive Domains of the Maxi-K Channel in the Mouse Myometrium during Gestation

Benkusky

Fergus

Zucchero

et al. 2000

Journal of Biological Chemistry

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Large conductance Ca(2+)-activated K(+) channels (maxi-K channels) are known to modulate uterine activity during gestation. Electrophysiological recordings demonstrate that myometrial maxi-K current is suppressed in term-pregnant compared to non-pregnant mice. We sought to determine whether maxi-K current suppression is due to reduction of maxi-K channel protein or differential expression of maxi-K channel isoforms that vary in their Ca(2+) and voltage sensitivities. Immunoblot analyses show an increase of maxi-K channel protein throughout gestation. Polymerase chain reaction of mouse myometrial cDNA identified four alternatively spliced sites within the maxi-K transcript and three within the Ca(2+)-sensitive "tail" domain. Ribonuclease protection analyses demonstrate that total channel transcript levels mimic protein expression; however transcript levels of alternatively spliced regions of regulatory domains that alter sensitivity to voltage and Ca(2+) differ in their gestational expression. An insert that increases the maxi-K channel sensitivity to voltage and Ca(2+) is present at steady levels throughout gestation, differing from total channel transcript regulation. The insert-less form of this transcript, which reduces the channel voltage and Ca(2+) sensitivity, is not detected until midterm pregnancy. These findings verify that multiple isoforms of the maxi-K channel are present in the mouse myometrium and are regulated differentially during gestation, which is a likely mechanism for modulation of myometrial excitability during pregnancy.

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Hormonal influence on ionic channels in myometrium

Cited by 10 publications

References 42 publications

Sex Hormones and Excitation–Contraction Coupling in the Uterus: The Effects of Oestrous and Hormones

Sex Hormones and Excitation–Contraction Coupling in the Uterus: The Effects of Oestrous and Hormones

The Effect of Progesterone on Myometrial Contractility, Potassium Channels, and Tocolytic Efficacy

Regulation of the Ca2+-sensitive Domains of the Maxi-K Channel in the Mouse Myometrium during Gestation

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