ArticleScientific reports2022
Characterization of the Dahl salt-sensitive rat as a rodent model of inherited, widespread, persistent pain.
Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 9 citations in OpenAlex.
- β-Hydroxybutyrate Attenuates Cardiac Inflammation and Hepatic Fibrosis in Dahl Salt-Sensitive Rats.Current issues in molecular biology · 2026Article
- Article
- Hypertension and brain damage: evidence from rodent models.Laboratory animal research · 2026Review
- Article
- Modeling Pain Without Injury: Inherited Rodent Models as Mechanistic Windows into Chronic Pain.Function (Oxford, England) · 2025Review
- Article
- Impact of homeostatic body hydration status, evaluated by hemodynamic measures, on different pain sensitization paths to a chronic pain syndrome.Scientific reports · 2024Article
- Descending Control of Nociception Poorly Predicts the Development of Persistent Postsurgical Pain-like Behavior in Consomic Dahl S Rat Strains.Anesthesiology · 2023Article
- Red Quinoa Hydrolysates with Antioxidant Properties Improve Cardiovascular Health in Spontaneously Hypertensive Rats.Antioxidants (Basel, Switzerland) · 2023Article
- Discovering chronic pain treatments: better animal models might help us get there.The Journal of clinical investigation · 2023Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Animal models are essential for studying the pathophysiology of chronic pain disorders and as screening tools for new therapies. However, most models available do not reproduce key characteristics of clinical persistent pain. This has limited their ability to accurately predict which new medicines will be clinically effective. Here, we characterize the Dahl salt-sensitive (SS) rat strain as the first rodent model of inherited widespread hyperalgesia. We show that this strain exhibits physiological phenotypes known to contribute to chronic pain, such as neuroinflammation, defective endogenous pain modulation, dysfunctional hypothalamic-pituitary-adrenal axis, increased oxidative stress and immune cell activation. When compared with Sprague Dawley and Brown Norway rats, SS rats have lower nociceptive thresholds due to increased inflammatory mediator concentrations, lower corticosterone levels, and high oxidative stress. Treatment with dexamethasone, the reactive oxygen species scavenger tempol, or the glial inhibitor minocycline attenuated the pain sensitivity in SS rats without affecting the other strains while indomethacin and gabapentin provided less robust pain relief. Moreover, SS rats presented impaired diffuse noxious inhibitory controls and an exacerbated response to the proalgesic mediator PGE
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