Evidence map›Paper›PMID 42472624›Full record

ArticleInternational neurourology journal2026

Effects of Oxytocin on Rats With Stress-Induced Increased Urinary Frequency.

Saori Nishijima, Katsumi Kadekawa, Katsuhiro Ashitomi, Seiji Matsumoto, Kimio Sugaya

Abstract read
In one paragraph

Article in International neurourology journal, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

What it found

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

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3 · Its place in the literature

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0 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

5 authors.

Saori NishijimaSouthern Knights' Laboratory, Okinawa, Japan. nishijima@sklabo.co.jp.
Katsumi KadekawaSouthern Knights' Laboratory, Okinawa, Japan.
Katsuhiro AshitomiSouthern Knights' Laboratory, Okinawa, Japan.
Seiji MatsumotoHeadquarters for Research Promotion, Asahikawa Medical University, Asahikawa, Japan.
Kimio SugayaSouthern Knights' Laboratory, Okinawa, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeUrinary frequency and bladder hypersensitivity are among the lower urinary tract symptoms exacerbated by psychological stress. This study investigated whether chronic oxytocin (OXT) administration could alleviate stress-induced bladder dysfunction and modulate central stress pathways.

methodsFemale Sprague-Dawley rats were allocated to control, stress, or stress/OXT groups (n=14 per group) and exposed to repeated variable stress (RVS) for 1 week. Assessments included mechanical sensitivity, cystometric parameters, plasma catecholamine and cortisol levels, bladder histology, c-Fos expression in the paraventricular nucleus (PVN), and gene expression in bladder and brain regions.

resultsRVS induced mechanical hypersensitivity, reduced intercontraction intervals, increased bladder weight, and raised plasma adrenaline, dopamine, and cortisol levels. The bladder also showed epithelial thickening, submucosal nerve hyperplasia, and increased prostaglandin E receptor 3 and epithelial sodium channel expression. Stress significantly enhanced PVN activation and increased brainstem expression of choline acetyltransferase, corticotropin-releasing factor, and tyrosine hydroxylase. With OXT treatment, intercontraction intervals normalized, catecholamine and cortisol levels declined, PVN c-Fos activation decreased, and OXT receptor expression increased in the brainstem, hypothalamus, and thalamus, and glutamate decarboxylase 1 expression increased in the hypothalamus and thalamus. Interleukin-6 expression decreased with OXT treatment but did not change in response to stress.

conclusionChronic OXT administration was associated with improved stress-induced urinary frequency and modulation of central stress pathways; evidence of direct peripheral anti-inflammatory effects was limited.

Indexed as

c-FosLower urinary tract symptomsOxytocinParaventricular hypothalamic nucleusStress-induced urinary frequency

Identifiers

PMID42472624
PMCPMC13643464

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.