Estrogen induced functional hypertrophy and increased force generation of the female rabbit bladder

Lin, Alpha Dian-Yu; Levin, Robert M.; Kogan, Barry A.; Whitbeck, Catherine; Chichester, Paul; Sokol, Rebekah; Mannikarottu, Anita

doi:10.1002/nau.20258

Cited by 41 publications

(49 citation statements)

References 21 publications

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“…The benefit that this ER repression may provide to the parasite could be explained by the following hypothesis: estradiol treatment as been shown to increase the smooth muscle density of the bladder in female rats. 88 In our study we observed downregulation of expression of ER in the smooth muscle of Sh-treated bladders. 88 During increase in gene expression, ERb mediates the large majority (nearly 90%) of estrogen-mediated decreases in gene expression.…”

Section: ©2 0 1 1 L a N D E S B I O S C I E N C E D O N O T D I S Tsupporting

confidence: 60%

“…88 In our study we observed downregulation of expression of ER in the smooth muscle of Sh-treated bladders. 88 During increase in gene expression, ERb mediates the large majority (nearly 90%) of estrogen-mediated decreases in gene expression. 80 Additionally, it is possible that Sh-induced ERa and b downregulation serves to control physiological responses in estrogen target tissues, which ultimately serves to limit the expression of estrogen responsive genes by the parasite.…”

Section: ©2 0 1 1 L a N D E S B I O S C I E N C E D O N O T D I S Tsupporting

confidence: 60%

“…Some authors reported that these species are able to covalently bind DNA bases, forming stable adducts. [86][87][88][89] These adducts can be considered as estrogen-bound metabolites generated in vitro that are produced by nucleophilic attack of the DNA base on different positions of the steroid ring. [89][90][91][92] Catechol estrogen-3,4-quinone adducts of DNA have been proposed as endogenous initiators of breast, prostate and other human cancers.…”

Section: ©2 0 1 1 L a N D E S B I O S C I E N C E D O N O T D I S Tmentioning

confidence: 99%

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Targeting molecular signaling pathways of Schistosoma haemotobium infection in bladder cancer

et al. 2011

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confidence: 60%

Section: ©2 0 1 1 L a N D E S B I O S C I E N C E D O N O T D I S Tsupporting

confidence: 60%

Section: ©2 0 1 1 L a N D E S B I O S C I E N C E D O N O T D I S Tmentioning

confidence: 99%

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Targeting molecular signaling pathways of Schistosoma haemotobium infection in bladder cancer

et al. 2011

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“…In addition to modulation of the urethral outlet function or as its consequence, E 2 has a strong effect on the bladder reservoir. Indeed, it can induce detrusor hypertrophy (16) or reduce the density of muscarinic receptors (25) in keeping with the significant improvement of overactive bladder symptoms in postmenopausal women (7).…”

Section: Discussionmentioning

confidence: 94%

Estradiol increases urethral tone through the local inhibition of neuronal nitric oxide synthase expression

Gamé¹,

Allard²,

Escourrou³

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

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Gamé X, Allard J, Escourrou G, Gourdy P, Tack I, Rischmann P, Arnal J-F, Malavaud B. Estradiol increases urethral tone through the local inhibition of neuronal nitric oxide synthase expression. Am J Physiol Regul Integr Comp Physiol 294: R851-R857, 2008. First published January 9, 2008 doi:10.1152/ajpregu.00467.2007.-Estrogens are known to modulate lower urinary tract (LUT) trophicity and neuronal nitric oxide synthase (nNOS) expression in several organs. The aim of this study was to explore the effects of endogenous and supraestrus levels of 17␤-estradiol (E2) on LUT and urethral nNOS expression and function. LUT function and histology and urethral nNOS expression were studied in adult female mice subjected either to sham surgery, surgical castration, or castration plus chronic E2 supplementation (80 g ⅐ kg Ϫ1 ⅐ day Ϫ1 , i.e., pregnancy level). The micturition pattern was profoundly altered by long-term supraestrus levels of E2 with decreased frequency paralleled by increased residual volumes higher than those of ovariectomized mice. Urethral resistance was increased twofold in E2-treated mice, with no structural changes in urethra, supporting a pure tonic mechanism. Acute nNOS inhibition by 7-nitroindazole decreased frequency and increased residual volumes in ovariectomized mice but had no additive effect on the micturition pattern of long-term supraestrus mice, showing that longterm supraestrus E2 levels and acute inhibition of nNOS activity had similar functional effects. Finally, E2 decreased urethral nNOS expression in ovariectomized mice. Long-term supraestrus levels of E2 increased urethral tone through inhibition of nNOS expression, whereas physiological levels of E2 had no effect. estrogen; neurourology; urethra UP TO 50% OF WOMEN ARE REPORTED to suffer from urinary incontinence or overactive bladder (22). Lower urinary tract function is intimately interrelated to physiological estradiol (E 2 ) variations, as illustrated by the transitory increase in urethral pressure at the peak of E 2 secretion at midcycle (32), its gradual increase during pregnancy (15), and the prevalence of urinary bothers after menopause (6).In woman, estrogen therapy has been shown to prevent postmenopausal cystitis (8) and urinary atrophy and overactive bladder (6). Moreover, clinical data suggest that estrogens partly improve lower urinary tract functioning by improving local trophicity (13). However, regarding urinary incontinence, estrogens either failed to show any effect on stress urinary incontinence (24) or actually increased (in a large multicentric study) the incidence and severity of all types of urinary incontinence (12).The intricate relationship between urine storage and micturition involves a reciprocal balance in the muscle tone of bladder and urethra, which are under spinal and supraspinal controls. Autonomic regulation of the lower urinary tract physiology is driven by all three components of the autonomic nervous system. Nitric oxide (NO), the key neurotransmitter of the nonadrenergic, noncholinergic nerves ...

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“…2 vP and uP in ovx control animals are considerably lower than in E2 treated animals which confirms our previous observation. The increased bladder and urethral pressure are most likely due to increased muscular activity as a higher muscle mass of the detrusor and sphincter and higher blood supply was reported in ovx-E2 in comparison to untreated animals (Aikawa et al, 2003;Lin et al, 2006a;Lin et al, 2006b;Lin et al, 2006c). It appears that the 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64 65 6 phytoestrogens have similar, though weaker effects in the detrusor than in the sphincter apparatus.…”

Section: Discussionmentioning

confidence: 95%

Comparison of urodynamic effects of phytoestrogens equol, puerarin and genistein with these of estradiol 17β in ovariectomized rats

Thielemann

Wuttke

et al. 2010

Experimental Gerontology

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Comparison of urodynamic effects of phytoestrogens equol, puerarin and genistein with these of estradiol 17β in ovariectomized rats. Experimental Gerontology, Elsevier, 2010, 45 (2) This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. ACCEPTED MANUSCRIPT AbstractWhether urinary incontinence in the postmenopause can be prevented or delayed by estrogens is currently controversially debated. Ovariectomized (ovx) rats have been successfully used as models in the past years but plant derived substances with estrogenic effects in the lower urinary tract have not been studied so far. Therefore we compared the effects of a 3 months lasting oral administration of estradiol 17ß (E2) with those of the phytoestrogens equol, genistein and puerarin. They were then anaesthetized and catheterized with a biluminal catheter having one outlet in the bladder and another in the urethra at the level of the urethral sphincter. Urethral and bladder pressure were recorded during a 240 sec period of retrograde bladder filling (2 x 0.5 ml within 30 s with 1 min filling intermission). Bladder and urethra pressures were highest in the E2>puerarin>equol>genistein treated animals. Phytoestrogen and E2 treatment resulted in consistently higher urethral than the bladder pressures during the filling period and in the filled status whereas bladder often exceeded urethral pressures in ovx controls. In summary, we demonstrate significant improvement of urethral closure mechanism under E2 and phytoestrogen administration that can be assumed to be beneficial for prevention or therapy of postmenopausal urge incontinence.

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Estrogen induced functional hypertrophy and increased force generation of the female rabbit bladder

Abstract: The present study demonstrates that estrogen supplementation mediates a "functional hypertrophy," that is a hypertrophy characterized by increased contractile responses to all forms of stimulation, and an increased ratio of SM/collagen.

Cited by 41 publications

References 21 publications

Targeting molecular signaling pathways of Schistosoma haemotobium infection in bladder cancer

Targeting molecular signaling pathways of Schistosoma haemotobium infection in bladder cancer

Estradiol increases urethral tone through the local inhibition of neuronal nitric oxide synthase expression

Comparison of urodynamic effects of phytoestrogens equol, puerarin and genistein with these of estradiol 17β in ovariectomized rats

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