ArticleJournal of neuroendocrinology2013
Compromise of endogenous neuropeptide W production abrogates the dipsogenic and pressor effects of angiotensin II in adult male rats.
Article in Journal of neuroendocrinology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed, 6 citations in OpenAlex.
- Thirst: neuroendocrine regulation in mammals.Veterinary research communications · 2023Review
- Identification of NPB, NPW and Their Receptor in the Rat Heart.International journal of molecular sciences · 2020Article
- Distribution and Function of Neuropeptides W/B Signaling System.Frontiers in physiology · 2018Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Neuropeptide W (NPW), an endogenous ligand for the G-protein coupled receptor GPR7, is produced in neurones in the rat hypothalamus and brain stem known to be important in the control of food intake and the neuroendocrine response to stress. In previous studies, central administration of NPW during the light phase increased food and water intake and elevated prolactin and corticosterone levels in conscious, unrestrained male rats. In the present study, central administration of small-interfering RNA (siRNA) reduced NPW levels in the hypothalamus and resulted in a failure of angiotensin II to stimulate water drinking or increase mean arterial pressure. In addition, siRNA-treated animals failed to mount a significant prolactin response to immobilisation stress, at the same time as maintaining a normal corticosterone response. These results suggest that endogenous NPW may be a physiologically relevant, downstream mediator of the central actions of angiotensin II to stimulate thirst and increase arterial pressure. In addition, NPW-producing neurones appear to participate in the hypothalamic mechanisms controlling prolactin (but not corticosterone) secretion.
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Registered trials
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.