Acute relaxation of mouse duodenun by estrogensEvidence for an estrogen receptor-independent modulation of muscle excitability

Dı́az, Mario; Ramírez, Cristina M.; Marín, Raquel; Marrero-Alonso, Jorge; Gómez, Tomás; Alonso, Rafael

doi:10.1016/s0014-2999(04)00932-x

Cited by 19 publications

(14 citation statements)

References 56 publications

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“…We also demonstrated that HSP27 protein expression was significantly elevated in intestinal muscles isolated from ovariectomized rats treated with 17-estradiol (control, 24.7  3.45%; 17-estradiol, 46.4  8.52%; P<0.05; n=6) DISCUSSION There are two types of estrogen receptor (ER), ER and ER, and ER is known to be expressed in intestinal tissues [9]. It has been reported that 17-estradiol inhibits contractions in intestinal smooth muscles [11], either by activating K + channels or by inhibiting Ca 2+ channels; however, these responses are considered to be triggered by an ER-independent mechanism [5]. Estrogen response sequences (ERS) exist in the transcriptional region of HSP27 [18], and the estrogen/ER complex binds directly to ERS, which results in induction of HSP27 transcription.…”

Section: Carbachol-induced Contraction Decreased With Upregulation Ofmentioning

confidence: 96%

“…These reports have indicated that estrogen may inhibit smooth muscle contractility via estorgen receptor (ER). In contrast, Diaz et al reported that the estrogen-induced acute inhibitory action of smooth muscle contraction operates through ER-independent modulation of muscle excitability via direct activation of K + channels and direct inhibition of voltage-dependent Ca 2+ channels [5]. Thus, the mechanisms of estrogen-induced motility disorder in intestinal smooth muscle remain controversial.…”

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confidence: 99%

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17.BETA.-Estradiol Induces Gastrointestinal Motility Disorder by Decreasing CPI-17 Phosphorylation Via Changes in Rho-Family G-Protein Rnd Expression in Small Intestine

2009

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ABSTRACT. In the present study, we investigated the long-term effects of 17-estradiol on the motility of small intestine in in vitro organ culture and in vivo treatment studies. When rat ileal circular smooth muscle tissues were cultured with 17-estradiol (0.1 and 1 M) for 5 days, carbachol-induced contraction was inhibited. In ileal tissue isolated from ovariectomized rat treated with 17-estradiol (200 g/ kg/day s.c. for 3 days), carbachol-induced contraction was also impaired. Both in vitro and in vivo, 17-estradiol treatment upregulated heat shock protein 27 (HSP27) expression, indicating the activation of estrogen receptor in the intestinal smooth muscle. 17-estradiol did not change protein expression levels of RhoA and RhoA-associated coiled coil-forming serine/threonine kinases (ROCKs); however, it upregulated Rnd2 and Rnd3, Rho-family G-proteins that counteract the functions of RhoA, both in vitro and in vivo. In organ culture, treatment of ileal tissue with 17-estradiol greatly suppressed the carbachol-induced increase in phosphorylation at Thr38 in CPI-17 without altering total CPI-17 protein expression. These results suggest that 17-estradiol upregulates Rnd expression to inhibit the RhoAmediated Ca 2+ sensitization of contractile mechanisms, which are mediated by CPI-17 phosphorylation in ileal smooth muscle. This mechanism may contribute to the intestinal motility disorder occurring in gender-dependent bowel diseases.

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Section: Carbachol-induced Contraction Decreased With Upregulation Ofmentioning

confidence: 96%

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confidence: 99%

17.BETA.-Estradiol Induces Gastrointestinal Motility Disorder by Decreasing CPI-17 Phosphorylation Via Changes in Rho-Family G-Protein Rnd Expression in Small Intestine

2009

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“…A similar effect was exerted also by verruculogen (Bikson et al, 2002). Being one of the most potent and selective, large conductance, calcium-sensitive potassium channel blocker, 5 was recently used as an effective pharmacological tool in studies aimed to explore role and function of this type of ionotropic receptors (Knaus et al, 1994;Akoi and Baraban, 2000;Diaz et al, 2004;Song and Marvizon, 2005;Khoufache et al, 2007;Smith et al, 2007;Waller et al, 2008). Fumitremorgin B 7 and verruculogen 5 were also shown to be genotoxic, causing DNA damage in Salmonella spp.…”

Section: Indole Alkaloidsmentioning

confidence: 98%

Chemistry and biological activity of azoprenylated secondary metabolites

2009

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“…These are relatively slow phenomena known as genomic effects ( Beato and Klug, 2000 ). In addition, several reports have demonstrated other effects of steroids with a rapid onset and short duration in some isolated cells and tissues, including brain ( McEwen, 1991 ; Brann et al , 1995 ), smooth muscles from cardiovascular ( Yue et al , 1995 ; Costarella et al , 1996 ; Jones et al , 2004 ), gastrointestinal ( Diaz et al , 2004 ), respiratory ( Kouloumenta et al , 2006 ) and genitourinary systems ( Perusquía et al , 2005 ) and other cell types ( Lösel et al , 2005 ). This rapid action is assumed to be non‐genomic, being initiated at the plasma membrane and supported by the existence of steroidal membrane receptors in several tissues ( Blackmore et al , 1991 ; Farach‐Carson and Davis, 2003 ; Lösel et al , 2005 ).…”

Section: Introductionmentioning

confidence: 99%

Evidence for the participation of calcium in non‐genomic relaxations induced by androgenic steroids in rat vas deferens

Lafayette

Vladimirova

Garcez-do-Carmo

et al. 2008

British J Pharmacology

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Background and purpose: Androgens cause non-genomic relaxation in several smooth muscle preparations. However, such an effect has not been investigated in rat vas deferens yet. Our purpose was to study the effect of testosterone and derivatives in this tissue. Experimental approach: The influence of androgens was tested on contraction and translocation of intracellular Ca 2 þ induced by KCl in rat vas deferens in vitro. Key results: The testosterone derivative 5a-dihydrotestosterone produced a rapid and reversible concentration-dependent relaxation of KCl-induced contractions. Other androgens were also effective, showing the following rank order of potency: androsterone 45b-dihydrotestosterone 4androstenedione 45a-dihydrotestosterone 4testosterone. Calcium-induced contractions were also inhibited (about 45%) by 5a-dihydrotestosterone (30 mM). Moreover 5a-dihydrotestosterone blocked the increase of intracellular Ca 2 þ induced by KCl, measured by the fluorescent dye fura-2. Relaxation to 5a-dihydrotestosterone was resistant to the K þ channel antagonists glibenclamide, 4-aminopyridine and charybdotoxin. It was not affected by removal of epithelium or by L-NNA (300 mM), an inhibitor of nitric oxide biosynthesis, nor by selective inhibitors of soluble guanylate cyclase, ODQ or LY 83583, indicating that nitrergic or cGMP mediated mechanisms were not involved. The androgen-induced relaxation was also not blocked by the protein synthesis inhibitor cycloheximide (300 mM) or by the classical androgen receptor flutamide (up to 100 mM), corroborating that the effect is non-genomic. Conclusions and implications: Testosterone derivatives caused relaxation of the rat vas deferens, that did not involve epithelial tissue, K þ channels, or nitric oxide-dependent mechanisms, but was related to a partial blockade of Ca 2 þ influx.

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Acute relaxation of mouse duodenun by estrogensEvidence for an estrogen receptor-independent modulation of muscle excitability

Cited by 19 publications

References 56 publications

17.BETA.-Estradiol Induces Gastrointestinal Motility Disorder by Decreasing CPI-17 Phosphorylation Via Changes in Rho-Family G-Protein Rnd Expression in Small Intestine

17.BETA.-Estradiol Induces Gastrointestinal Motility Disorder by Decreasing CPI-17 Phosphorylation Via Changes in Rho-Family G-Protein Rnd Expression in Small Intestine

Chemistry and biological activity of azoprenylated secondary metabolites

Evidence for the participation of calcium in non‐genomic relaxations induced by androgenic steroids in rat vas deferens

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