The renin–angiotensin system plays a major role in voiding dysfunction of ovariectomized rats

Ramos-Filho, Antonio Celso Saragossa; Faria, Juliana A.; Calmasini, Fabiano Beraldi; Teixeira, Simone Aparecida; Mónica, Fabíola Z.; Muscará, Marcelo Nícolas; Gontijo, José Antônio Rocha; Anhê, Gabriel Forato; Zanesco, Angelina; Antunes, Edson

doi:10.1016/j.lfs.2013.09.008

Cited by 13 publications

(11 citation statements)

References 54 publications

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“…Moreover, the frequency score was significantly improved in the group receiving combined medications that included AT1R antagonists 17 . Previous preclinical research demonstrated that peripheral Ang II causes urethral contractions in a dose-dependent manner, and that chronic treatment with an AT1R antagonist, losartan, reduces urinary frequency in ovariectomised oestrogen-deficient rats 18 . Furthermore, Comiter et al reported that losartan partially prevents urodynamic and structural changes associated with bladder obstruction in the mouse 19 .…”

Section: Discussionmentioning

confidence: 99%

Angiotensin II centrally induces frequent detrusor contractility of the bladder by acting on brain angiotensin II type 1 receptors in rats

Kawamoto

Shimizu

et al. 2016

Sci Rep

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Angiotensin (Ang) II plays an important role in the brain as a neurotransmitter and is involved in psychological stress reactions, for example through activation of the sympatho-adrenomedullary system. We investigated the effects of centrally administered Ang II on the micturition reflex, which is potentially affected by the sympatho-adrenomedullary system, and brain Ang II receptors in urethane-anesthetized (1.0 g/kg, intraperitoneally) male rats. Central administration of Ang II (0.01, 0.02, and 0.07 nmol per rat, intracerebroventricularly, icv) but not vehicle rapidly and dose-dependently decreased the urinary bladder intercontraction interval, without altering the bladder detrusor pressure. Central administration of antagonists of Ang II type 1 but not type 2 receptors inhibited the Ang II-induced shortening of intercontraction intervals. Administration of the highest dose of Ang II (0.07 nmol per rat, icv) but not lower doses (0.01 and 0.02 nmol per rat, icv) elevated the plasma concentration of adrenaline. Bilateral adrenalectomy reduced Ang II-induced elevation in adrenaline, but had no effect on the Ang II-induced shortening of the intercontraction interval. These data suggest that central administration of Ang II increases urinary frequency by acting on brain Ang II type 1 receptors, independent of activation of the sympatho-adrenomedullary system.

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Section: Discussionmentioning

confidence: 99%

Angiotensin II centrally induces frequent detrusor contractility of the bladder by acting on brain angiotensin II type 1 receptors in rats

Kawamoto

Shimizu

et al. 2016

Sci Rep

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“…17,18 However, estrogen is shown to exert a tissue-specific effect by regulating AT 2 R expression in the kidneys 17,18 but not in lungs, 19 urethra, 20 and blood vessels. 17 On the other hand, whether androgens exert control on AT 2 R expression is unknown.…”

Section: Introductionmentioning

confidence: 99%

Testosterone downregulates angiotensin II type-2 receptor via androgen receptor-mediated ERK1/2 MAP kinase pathway in rat aorta

Mishra

Hankins

Kumar

2016

J Renin Angiotensin Aldosterone Syst

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Introduction Blood pressure is lower in females than males. Angiotensin II type-2 receptor (AT2R) induces vasodilation. This study determined whether sex differences in vascular AT2R expression occur and if androgens exert control on AT2R expression in the vasculature. Methods AT2Rs in the aorta of male and female Sprague-Dawley rats were examined following alteration in androgen levels by gonadectomy or hormone supplementation. Results AT2R mRNA and protein expression levels were lower in aorta of males than females. In males, testosterone withdrawal by castration significantly elevated AT2R mRNA and protein levels and testosterone replacement restored them. In females, increasing androgen levels decreased AT2R mRNA and protein expression and this was attenuated by androgen receptor blocker flutamide. Ex vivo, dihydrotestosterone downregulated AT2R in endothelium-intact but not -denuded aorta. Dihydrotestosterone-induced AT2R downregulation in isolated aorta was blocked by androgen receptor antagonist. Furthermore, blockade of ERK1/2 but not p38 MAP kinase or TGFβ signaling with specific inhibitors abolished dihydrotestosterone-induced AT2R downregulation. Conclusion Androgens downregulates AT2R expression levels in aorta, in vivo and ex vivo. The androgen receptor-mediated ERK1/2 MAP kinase-signaling pathway may be a key mechanism by which testosterone downregulates AT2R expression, implicating androgens’ contributing role to gender differences in vascular AT2R expression.

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“…The main pathomechanisms for this seem to be increased angiotensin-converting enzyme (ACE) activity and up-regulation of AT1 and AT2 receptors. 4 Furthermore, Cho et al 5 described the role of AT1 receptors in the development of detrusor overactivity (DO) due to bladder outlet obstruction (BOO) in a rat model. The function of AT1 receptors in DO remain unclear.…”

mentioning

confidence: 99%

The angiotensin II receptors type 1 blockage affects the urinary bladder activity in hyperosmolar-induced detrusor overactivity in rats: Preliminary results

Juszczak¹,

Maciukiewicz²

2017

Adv Clin Exp Med

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The renin–angiotensin system plays a major role in voiding dysfunction of ovariectomized rats

Cited by 13 publications

References 54 publications

Angiotensin II centrally induces frequent detrusor contractility of the bladder by acting on brain angiotensin II type 1 receptors in rats

Angiotensin II centrally induces frequent detrusor contractility of the bladder by acting on brain angiotensin II type 1 receptors in rats

Testosterone downregulates angiotensin II type-2 receptor via androgen receptor-mediated ERK1/2 MAP kinase pathway in rat aorta

The angiotensin II receptors type 1 blockage affects the urinary bladder activity in hyperosmolar-induced detrusor overactivity in rats: Preliminary results

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