Estradiol rapidly induces the translocation and activation of the intermediate conductance calcium activated potassium channel in human eccrine sweat gland cells

Muchekehu, Ruth W.; Harvey, Bill

doi:10.1016/j.steroids.2008.10.013

Cited by 14 publications

(9 citation statements)

References 25 publications

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“…It is likely that this expression is occurring within the endothelium as studies show localization of this channel exclusively to the endothelium of rat and murine blood vessels (Edwards et al ., 1998; Doughty et al ., 1999; Walker et al ., 2001; Brahler et al ., 2009) and human endothelial cells of mesenteric arteries (Kohler et al ., 2000). In support of the concept that oestrogens influence K Ca 3.1 channels, recent studies in the human sweat gland epithelial cell line NCL‐SG3 have shown that oestrogen treatment rapidly activates a whole cell K + current mediated through K Ca 3.1 channels that is independent of oestrogen receptor activation and a consequence of the rapid translocation of K Ca 3.1 channels to the cell membrane (Muchekehu and Harvey, 2009). Whether such translocation might also underlie the female sex hormone‐dependent effects in the present study is uncertain and warrants investigation.…”

Section: Discussionmentioning

confidence: 94%

Distinct endothelial pathways underlie sexual dimorphism in vascular auto‐regulation

Chan

Bubb

Noyce

et al. 2012

British J Pharmacology

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BACKGROUND AND PURPOSEPre-menopausal females have a lower incidence of cardiovascular disease compared with age-matched males, implying differences in the mechanisms and pathways regulating vasoactivity. In small arteries, myogenic tone (constriction in response to raised intraluminal pressure) is a major determinant of vascular resistance. Endothelium-derived dilators, particularly NO, tonically moderate myogenic tone and, because the endothelium is an important target for female sex hormones, we investigated whether NO-mediated moderation of myogenic tone differed between the sexes. EXPERIMENTAL APPROACHPressure-diameter or relaxation concentration-response curves to the NO donor spermine-NO or soluble guanylate cyclase (sGC) stimulation (BAY41-2272) were constructed before and following drug intervention in murine mesenteric resistance arteries. Hypotensive responses to activators of the NO-sGC pathway were determined. Quantitative PCR and Western blotting were used for expression analysis. KEY RESULTSNO synthase inhibition enhanced myogenic tone of arteries of both sexes while block of endothelium-derived hyperpolarizing factor (EDHF) enhanced responses in arteries of females only. Spermine-NO concentration-dependently relaxed mesenteric arteries isolated from either sex. However, while inhibition of sGC activity attenuated responses of arteries from male mice only, endothelial denudation attenuated responses of arteries from females only. BAY41-2272 and spermine-NO-induced vasodilatation and hypotension were greater in males than in females. CONCLUSIONS AND IMPLICATIONSNO moderated myogenic tone in arteries of male mice by a sGC-dependent pathway while EDHF was the predominant endothelial regulator in arteries of females. This is a potentially important sexual dimorphism in NO-mediated reactivity and further implicates EDHF as the predominant endothelial vasodilator in female resistance arteries.

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Section: Discussionmentioning

confidence: 94%

Distinct endothelial pathways underlie sexual dimorphism in vascular auto‐regulation

Chan

Bubb

Noyce

et al. 2012

British J Pharmacology

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“…Ovarian hormones can act either by a genomic mechanism, using classical nuclear transcription factor receptors requiring at least 30-60 minutes to be manifest and is associated with changes in protein synthesis (38), or by a non-genomic, less well-characterized, rapid (seconds to minutes) membrane receptor signaling mechanism (39-42). Steroid- bovine serum albumin (BSA) conjugates are useful tools to study the membrane-mediated action of steroids since they are biologically active and do not penetrate readily the plasma membrane of the cell (43,44).…”

Section: Discussionmentioning

confidence: 99%

Comparison of the Effects of Estradiol and Progesterone on Serotonergic Function

Benmansour

Weaver

Barton

et al. 2012

Biological Psychiatry

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Background Ovarian hormones may contribute to the vulnerability to depression as well as to the response to antidepressants (ADs). Previously we reported that acute systemic treatment with estradiol or progesterone blocked the ability of the selective serotonin reuptake inhibitor (SSRI), fluvoxamine, to inhibit serotonin transporter (SERT) function in ovariectomized (OVX) rats. In this study, behavioral consequences as well as receptor mechanisms underlying these hormonal effects were investigated. Methods Using the forced swimming test (FST), the acute effect of estradiol and/or progesterone on fluvoxamine’s AD-like effects was investigated. Using in vivo chronoamperometry, the effect of local application of estradiol or progesterone into the CA3 region of the hippocampus of OVX rats on 5-HT clearance as well as on the ability of fluvoxamine to slow 5-HT clearance was investigated. Results The decreased immobility and increased swimming caused by fluvoxamine in the FST was blocked in rats treated with estradiol and/or progesterone. Local application of estradiol, but not progesterone, slowed 5-HT clearance and both hormones blocked the ability of fluvoxamine to slow 5-HT clearance. Use of hormone receptor agonists, antagonists and hormone-BSA complexes revealed that the effects of estradiol are mediated by activation of membrane as well as nuclear estrogen receptors (ER). The AD-like effect of estradiol involved ERβ and GPR30 whereas its blockade of fluvoxamine’s effects was ERα-mediated. The effects of progesterone occurred solely by activation of intracellular progesterone receptors. Conclusion Targeting of ERβ or GPR30 might reveal a strategy to permit beneficial effects of estrogen without its deleterious effect on SSRI-efficacy.

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“…Although non‐genomic effects of oestrogen are known to occur2–5 and mechanisms of action have been investigated extensively16, the exact cascades involved in the extranuclear signalling remain elusive and most probably vary between tissue types. The current hypothesis is that ORs close to the plasma membrane undergo conformational change after binding with oestradiol and modulate ion channels17, G proteins18 and tyrosine kinases19, leading to the activation of downstream messenger systems, such as mitogen‐activated protein kinases20 and phosphatidylinositol 3‐hydroxy kinase21, allowing the oestrogenic effect to be exerted. Recent studies have pointed to the specific and selective binding of steroid hormones to protein kinase C isoforms22.…”

Section: Introductionmentioning

confidence: 99%

Oestrogen inhibits human colonic motility by a non-genomic cell membrane receptor-dependent mechanism

Hogan

Kennelly

Collins

et al. 2009

British Journal of Surgery

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Estradiol rapidly induces the translocation and activation of the intermediate conductance calcium activated potassium channel in human eccrine sweat gland cells

Cited by 14 publications

References 25 publications

Distinct endothelial pathways underlie sexual dimorphism in vascular auto‐regulation

Distinct endothelial pathways underlie sexual dimorphism in vascular auto‐regulation

Comparison of the Effects of Estradiol and Progesterone on Serotonergic Function

Oestrogen inhibits human colonic motility by a non-genomic cell membrane receptor-dependent mechanism

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