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Detrusor underactivity causes neurogenic voiding dysfunction in a rat bilateral accessory nerve-injury model.

Abstract
We aimed to investigate detrusor function in a previously developed rat neurogenic voiding dysfunction model that we have developed previously. We performed sham or bilateral accessory nerve injury (BACNI) surgeries on ten-week-old male Wistar/ST rats. One week after surgery, we evaluated detrusor contractility in the bladder using isometric tension and mRNA expression assays. Cholinergic contraction was attenuated in the injury model, whereas carbachol-evoked contraction was enhanced, and mRNA expression of the cholinergic receptor increased. These findings suggest that there was a reduction in neurotransmitter release causing detrusor underactivity.
AuthorsKotomi Maeda, Yuji Hotta, Ryoya Kawata, Tomoya Kataoka, Kazunori Kimura
JournalJournal of pharmacological sciences (J Pharmacol Sci) Vol. 146 Issue 2 Pg. 116-119 (Jun 2021) ISSN: 1347-8648 [Electronic] Japan
PMID33941322 (Publication Type: Journal Article)
CopyrightCopyright © 2021 The Authors. Production and hosting by Elsevier B.V. All rights reserved.
Chemical References
  • Neurotransmitter Agents
  • RNA, Messenger
  • Receptors, Cholinergic
  • Carbachol
Topics
  • Accessory Nerve Injuries (complications)
  • Animals
  • Carbachol (pharmacology)
  • Disease Models, Animal
  • Gene Expression
  • Isometric Contraction (drug effects, genetics)
  • Male
  • Neurotransmitter Agents (metabolism)
  • RNA, Messenger (genetics, metabolism)
  • Rats, Wistar
  • Receptors, Cholinergic (metabolism)
  • Urinary Bladder (physiopathology)
  • Urinary Bladder, Neurogenic
  • Urinary Bladder, Underactive (complications, physiopathology)

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