Urinary reabsorption in the rat kidney by anticholinergics

Abstract Anticholinergics, therapeutic agents for overactive bladder, are clinically suggested to reduce urine output. We investigated whether this effect is due to bladder or kidney urine reabsorption. Various solutions were injected into the bladder of urethane-anesthetized SD rats. The absorption...

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Autores principales:	Hideki Oe, Hatsumi Yoshiki, Xinmin Zha, Hisato Kobayashi, Yoshitaka Aoki, Hideaki Ito, Osamu Yokoyama
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/a3eab46303b0499aabd4043c3a0be1ef
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spelling	oai:doaj.org-article:a3eab46303b0499aabd4043c3a0be1ef2021-12-02T17:39:33ZUrinary reabsorption in the rat kidney by anticholinergics10.1038/s41598-021-88738-y2045-2322https://doaj.org/article/a3eab46303b0499aabd4043c3a0be1ef2021-04-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-88738-yhttps://doaj.org/toc/2045-2322Abstract Anticholinergics, therapeutic agents for overactive bladder, are clinically suggested to reduce urine output. We investigated whether this effect is due to bladder or kidney urine reabsorption. Various solutions were injected into the bladder of urethane-anesthetized SD rats. The absorption rate for 2 h was examined following the intravenous administration of the anticholinergics imidafenacin (IM), atropine (AT), and tolterodine (TO). The bilateral ureter was then canulated and saline was administered to obtain a diuretic state. Anticholinergics or 1-deamino-[8-D-arginine]-vasopressin (dDAVP) were intravenously administered. After the IM and dDAVP administrations, the rat kidneys were immunostained with AQP2 antibody, and intracellular cAMP was measured. The absorption rate was ~ 10% of the saline injected into the bladder and constant even when anticholinergics were administered. The renal urine among peaked 2 h after the saline administration. Each of the anticholinergics significantly suppressed the urine production in a dose-dependent manner, as did dDAVP. IM and dDAVP increased the intracellular cAMP levels and caused the AQP2 molecule to localize to the collecting duct cells' luminal side. The urinary reabsorption mechanism through the bladder epithelium was not activated by anticholinergic administration. Thus, anticholinergics suppress urine production via an increase in urine reabsorption in the kidneys' collecting duct cells via AQP2.Hideki OeHatsumi YoshikiXinmin ZhaHisato KobayashiYoshitaka AokiHideaki ItoOsamu YokoyamaNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-10 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Hideki Oe Hatsumi Yoshiki Xinmin Zha Hisato Kobayashi Yoshitaka Aoki Hideaki Ito Osamu Yokoyama Urinary reabsorption in the rat kidney by anticholinergics
description	Abstract Anticholinergics, therapeutic agents for overactive bladder, are clinically suggested to reduce urine output. We investigated whether this effect is due to bladder or kidney urine reabsorption. Various solutions were injected into the bladder of urethane-anesthetized SD rats. The absorption rate for 2 h was examined following the intravenous administration of the anticholinergics imidafenacin (IM), atropine (AT), and tolterodine (TO). The bilateral ureter was then canulated and saline was administered to obtain a diuretic state. Anticholinergics or 1-deamino-[8-D-arginine]-vasopressin (dDAVP) were intravenously administered. After the IM and dDAVP administrations, the rat kidneys were immunostained with AQP2 antibody, and intracellular cAMP was measured. The absorption rate was ~ 10% of the saline injected into the bladder and constant even when anticholinergics were administered. The renal urine among peaked 2 h after the saline administration. Each of the anticholinergics significantly suppressed the urine production in a dose-dependent manner, as did dDAVP. IM and dDAVP increased the intracellular cAMP levels and caused the AQP2 molecule to localize to the collecting duct cells' luminal side. The urinary reabsorption mechanism through the bladder epithelium was not activated by anticholinergic administration. Thus, anticholinergics suppress urine production via an increase in urine reabsorption in the kidneys' collecting duct cells via AQP2.
format	article
author	Hideki Oe Hatsumi Yoshiki Xinmin Zha Hisato Kobayashi Yoshitaka Aoki Hideaki Ito Osamu Yokoyama
author_facet	Hideki Oe Hatsumi Yoshiki Xinmin Zha Hisato Kobayashi Yoshitaka Aoki Hideaki Ito Osamu Yokoyama
author_sort	Hideki Oe
title	Urinary reabsorption in the rat kidney by anticholinergics
title_short	Urinary reabsorption in the rat kidney by anticholinergics
title_full	Urinary reabsorption in the rat kidney by anticholinergics
title_fullStr	Urinary reabsorption in the rat kidney by anticholinergics
title_full_unstemmed	Urinary reabsorption in the rat kidney by anticholinergics
title_sort	urinary reabsorption in the rat kidney by anticholinergics
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/a3eab46303b0499aabd4043c3a0be1ef
work_keys_str_mv	AT hidekioe urinaryreabsorptionintheratkidneybyanticholinergics AT hatsumiyoshiki urinaryreabsorptionintheratkidneybyanticholinergics AT xinminzha urinaryreabsorptionintheratkidneybyanticholinergics AT hisatokobayashi urinaryreabsorptionintheratkidneybyanticholinergics AT yoshitakaaoki urinaryreabsorptionintheratkidneybyanticholinergics AT hideakiito urinaryreabsorptionintheratkidneybyanticholinergics AT osamuyokoyama urinaryreabsorptionintheratkidneybyanticholinergics
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Urinary reabsorption in the rat kidney by anticholinergics

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