ArticleBritish journal of pharmacology2018
Angiotensin II, a stress-related neuropeptide in the CNS, facilitates micturition reflex in rats.
Article in British journal of pharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 13 citations in OpenAlex.
- Persistent sleep symptoms in post-COVID syndrome: a Brazilian prospective clinical study.Arquivos de neuro-psiquiatria · 2025Observational
- Brain carbon monoxide can suppress the rat micturition reflex through brain γ-aminobutyric acid receptors.International journal of urology : official journal of the Japanese Urological Association · 2024Article
- Review
- Angiotensin II, a stress-related neuropeptide in the CNS, facilitates micturition reflex in rats.British journal of pharmacology · 2018Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeWe investigated the effects of centrally administered stress-related neuropeptide, angiotensin II, on the micturition reflex and the downstream signalling pathways in rats. EXPERIMENTAL APPROACH: Male Wistar rats were anaesthetized with urethane for cystometry before and after i.c.v. administration of vehicle or angiotensin II (30 pmol). Muscimol (a GABA KEY
resultsCentrally administered angiotensin II significantly shortened the intercontraction interval and decreased the voided volume and bladder capacity without altering the maximum voiding pressure, post-voiding residual urine volume or voiding efficacy. Muscimol, baclofen, telmisartan, valsartan, U-73122, chelerythrine chloride, apocynin or tempol pretreatment significantly suppressed the reduction in intercontraction interval induced by central angiotensin II. Post-treatment with muscimol or baclofen also ameliorated the decrease in intercontraction interval induced by central angiotensin II. CONCLUSIONS AND IMPLICATIONS: Angiotensin II in the CNS facilitates micturition reflex by inhibiting central GABAergic activity and activating the AT
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