Zolpidem increases bladder capacity and decreases urine excretion in rats

Aims To clarify the effects of zolpidem, a γ‐aminobutyric acid (GABA)A receptor agonist, on bladder function, and urine production, we investigated the effects of zolpidem administration on bladder overactivity induced by cerebral infarction (CI) and on urine excretion increased by water overloading...

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Veröffentlicht in:Neurourology and urodynamics 2010-04, Vol.29 (4), p.587-591
Hauptverfasser: Yokoyama, Osamu, Matsuta, Yosuke, Yanai-Inamura, Hiroko, Watanabe, Mai, Ohtake, Akiyoshi, Suzuki, Masanori, Sasamata, Masao
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container_end_page 591
container_issue 4
container_start_page 587
container_title Neurourology and urodynamics
container_volume 29
creator Yokoyama, Osamu
Matsuta, Yosuke
Yanai-Inamura, Hiroko
Watanabe, Mai
Ohtake, Akiyoshi
Suzuki, Masanori
Sasamata, Masao
description Aims To clarify the effects of zolpidem, a γ‐aminobutyric acid (GABA)A receptor agonist, on bladder function, and urine production, we investigated the effects of zolpidem administration on bladder overactivity induced by cerebral infarction (CI) and on urine excretion increased by water overloading in Wistar rats. Methods CI was induced by left middle cerebral artery occlusion. The effects on bladder function of zolpidem alone or in combination with the GABAA receptor antagonist bicuculline, were then examined in the CI rats using cystometry. The antidiuretic effect of zolpidem was investigated in water‐loaded and Brattleboro rats (genetically vasopressin‐deficient). Blood samples were collected from water‐loaded rats to determine the aldosterone level 1 and 6 hr after zolpidem administration. Results Zolpidem increased bladder capacity dose‐dependently, but had no significant effect on bladder contraction pressure in CI rats. Bicuculline dose‐dependently inhibited zolpidem‐induced increases in bladder capacity without affecting bladder contraction pressure. Zolpidem dose‐dependently decreased the volume of urine excreted in water‐loaded and Brattleboro rats. Compared with the control group, zolpidem significantly increased the aldosterone concentration in the plasma of water‐loaded rats 1 hr after administration. Conclusions Zolpidem increased bladder capacity via a GABAergic mechanism in CI rats, and suppressed urine excretion via a pathway that was not through activation of vasopressin V2 receptors in water‐loaded and Brattleboro rats. These results suggest that zolpidem may improve nocturia via an increase in bladder capacity and a decrease in urine excretion. Neurourol. Urodynam. 29:587–591, 2010. © 2009 Wiley‐Liss, Inc.
doi_str_mv 10.1002/nau.20797
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Methods CI was induced by left middle cerebral artery occlusion. The effects on bladder function of zolpidem alone or in combination with the GABAA receptor antagonist bicuculline, were then examined in the CI rats using cystometry. The antidiuretic effect of zolpidem was investigated in water‐loaded and Brattleboro rats (genetically vasopressin‐deficient). Blood samples were collected from water‐loaded rats to determine the aldosterone level 1 and 6 hr after zolpidem administration. Results Zolpidem increased bladder capacity dose‐dependently, but had no significant effect on bladder contraction pressure in CI rats. Bicuculline dose‐dependently inhibited zolpidem‐induced increases in bladder capacity without affecting bladder contraction pressure. Zolpidem dose‐dependently decreased the volume of urine excreted in water‐loaded and Brattleboro rats. Compared with the control group, zolpidem significantly increased the aldosterone concentration in the plasma of water‐loaded rats 1 hr after administration. Conclusions Zolpidem increased bladder capacity via a GABAergic mechanism in CI rats, and suppressed urine excretion via a pathway that was not through activation of vasopressin V2 receptors in water‐loaded and Brattleboro rats. These results suggest that zolpidem may improve nocturia via an increase in bladder capacity and a decrease in urine excretion. Neurourol. Urodynam. 29:587–591, 2010. © 2009 Wiley‐Liss, Inc.</description><identifier>ISSN: 0733-2467</identifier><identifier>EISSN: 1520-6777</identifier><identifier>DOI: 10.1002/nau.20797</identifier><identifier>PMID: 19760758</identifier><language>eng</language><publisher>Hoboken: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>Aldosterone - blood ; Animals ; Bicuculline - pharmacology ; bladder capacity ; Cerebral Infarction - complications ; Cerebral Infarction - physiopathology ; Disease Models, Animal ; Dose-Response Relationship, Drug ; Drug Therapy, Combination ; Female ; GABA Agonists - administration &amp; dosage ; GABA Agonists - pharmacology ; GABA Antagonists - pharmacology ; Infarction, Middle Cerebral Artery - complications ; Injections, Intravenous ; nocturia ; nocturnal polyuria ; Pyridines - administration &amp; dosage ; Pyridines - pharmacology ; Rats ; Rats, Brattleboro ; Rats, Sprague-Dawley ; Rats, Wistar ; Time Factors ; Urinary Bladder - drug effects ; Urinary Bladder - physiopathology ; Urinary Bladder, Overactive - drug therapy ; Urinary Bladder, Overactive - etiology ; Urinary Bladder, Overactive - physiopathology ; Urination - drug effects ; urine excretion ; Urodynamics ; zolpidem</subject><ispartof>Neurourology and urodynamics, 2010-04, Vol.29 (4), p.587-591</ispartof><rights>Copyright © 2009 Wiley‐Liss, Inc.</rights><rights>(c) 2009 Wiley-Liss, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4287-df6dd820770678ad13f2c41b0ebf39a92b61a350322533503cb16046bda5ecbb3</citedby><cites>FETCH-LOGICAL-c4287-df6dd820770678ad13f2c41b0ebf39a92b61a350322533503cb16046bda5ecbb3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fnau.20797$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fnau.20797$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19760758$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yokoyama, Osamu</creatorcontrib><creatorcontrib>Matsuta, Yosuke</creatorcontrib><creatorcontrib>Yanai-Inamura, Hiroko</creatorcontrib><creatorcontrib>Watanabe, Mai</creatorcontrib><creatorcontrib>Ohtake, Akiyoshi</creatorcontrib><creatorcontrib>Suzuki, Masanori</creatorcontrib><creatorcontrib>Sasamata, Masao</creatorcontrib><title>Zolpidem increases bladder capacity and decreases urine excretion in rats</title><title>Neurourology and urodynamics</title><addtitle>Neurourol. Urodyn</addtitle><description>Aims To clarify the effects of zolpidem, a γ‐aminobutyric acid (GABA)A receptor agonist, on bladder function, and urine production, we investigated the effects of zolpidem administration on bladder overactivity induced by cerebral infarction (CI) and on urine excretion increased by water overloading in Wistar rats. Methods CI was induced by left middle cerebral artery occlusion. The effects on bladder function of zolpidem alone or in combination with the GABAA receptor antagonist bicuculline, were then examined in the CI rats using cystometry. The antidiuretic effect of zolpidem was investigated in water‐loaded and Brattleboro rats (genetically vasopressin‐deficient). Blood samples were collected from water‐loaded rats to determine the aldosterone level 1 and 6 hr after zolpidem administration. Results Zolpidem increased bladder capacity dose‐dependently, but had no significant effect on bladder contraction pressure in CI rats. Bicuculline dose‐dependently inhibited zolpidem‐induced increases in bladder capacity without affecting bladder contraction pressure. Zolpidem dose‐dependently decreased the volume of urine excreted in water‐loaded and Brattleboro rats. Compared with the control group, zolpidem significantly increased the aldosterone concentration in the plasma of water‐loaded rats 1 hr after administration. Conclusions Zolpidem increased bladder capacity via a GABAergic mechanism in CI rats, and suppressed urine excretion via a pathway that was not through activation of vasopressin V2 receptors in water‐loaded and Brattleboro rats. These results suggest that zolpidem may improve nocturia via an increase in bladder capacity and a decrease in urine excretion. Neurourol. 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Urodyn</addtitle><date>2010-04</date><risdate>2010</risdate><volume>29</volume><issue>4</issue><spage>587</spage><epage>591</epage><pages>587-591</pages><issn>0733-2467</issn><eissn>1520-6777</eissn><abstract>Aims To clarify the effects of zolpidem, a γ‐aminobutyric acid (GABA)A receptor agonist, on bladder function, and urine production, we investigated the effects of zolpidem administration on bladder overactivity induced by cerebral infarction (CI) and on urine excretion increased by water overloading in Wistar rats. Methods CI was induced by left middle cerebral artery occlusion. The effects on bladder function of zolpidem alone or in combination with the GABAA receptor antagonist bicuculline, were then examined in the CI rats using cystometry. The antidiuretic effect of zolpidem was investigated in water‐loaded and Brattleboro rats (genetically vasopressin‐deficient). Blood samples were collected from water‐loaded rats to determine the aldosterone level 1 and 6 hr after zolpidem administration. Results Zolpidem increased bladder capacity dose‐dependently, but had no significant effect on bladder contraction pressure in CI rats. Bicuculline dose‐dependently inhibited zolpidem‐induced increases in bladder capacity without affecting bladder contraction pressure. Zolpidem dose‐dependently decreased the volume of urine excreted in water‐loaded and Brattleboro rats. Compared with the control group, zolpidem significantly increased the aldosterone concentration in the plasma of water‐loaded rats 1 hr after administration. Conclusions Zolpidem increased bladder capacity via a GABAergic mechanism in CI rats, and suppressed urine excretion via a pathway that was not through activation of vasopressin V2 receptors in water‐loaded and Brattleboro rats. These results suggest that zolpidem may improve nocturia via an increase in bladder capacity and a decrease in urine excretion. Neurourol. Urodynam. 29:587–591, 2010. © 2009 Wiley‐Liss, Inc.</abstract><cop>Hoboken</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>19760758</pmid><doi>10.1002/nau.20797</doi><tpages>5</tpages></addata></record>
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subjects Aldosterone - blood
Animals
Bicuculline - pharmacology
bladder capacity
Cerebral Infarction - complications
Cerebral Infarction - physiopathology
Disease Models, Animal
Dose-Response Relationship, Drug
Drug Therapy, Combination
Female
GABA Agonists - administration & dosage
GABA Agonists - pharmacology
GABA Antagonists - pharmacology
Infarction, Middle Cerebral Artery - complications
Injections, Intravenous
nocturia
nocturnal polyuria
Pyridines - administration & dosage
Pyridines - pharmacology
Rats
Rats, Brattleboro
Rats, Sprague-Dawley
Rats, Wistar
Time Factors
Urinary Bladder - drug effects
Urinary Bladder - physiopathology
Urinary Bladder, Overactive - drug therapy
Urinary Bladder, Overactive - etiology
Urinary Bladder, Overactive - physiopathology
Urination - drug effects
urine excretion
Urodynamics
zolpidem
title Zolpidem increases bladder capacity and decreases urine excretion in rats
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