ArticlePloS one2012
N-octanoyl-dopamine is an agonist at the capsaicin receptor TRPV1 and mitigates ischemia-induced [corrected] acute kidney injury in rat.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 42 citations in OpenAlex.
- Spice Up Your Kidney: A Review on the Effects of Capsaicin in Renal Physiology and Disease.International journal of molecular sciences · 2024Review
- Therapeutic Potential of Dopamine and Related Drugs as Anti-Inflammatories and Antioxidants in Neuronal and Non-Neuronal Pathologies.Pharmaceutics · 2023Review
- Capsaicin Prevents Contrast-Associated Acute Kidney Injury through Activation of Nrf2 in Mice.Oxidative medicine and cellular longevity · 2022Article
- Transient receptor potential vanilloid subtype 1: A potential therapeutic target for fibrotic diseases.Frontiers in physiology · 2022Review
- Endocannabinoid System in Polycystic Kidney Disease.American journal of nephrology · 2022Article
- TRPV1 Hyperfunction Contributes to Renal Inflammation in Oxalate Nephropathy.International journal of molecular sciences · 2021Article
- Cannabinoid Receptor 1 Inhibition in Chronic Kidney Disease: A New Therapeutic Toolbox.Frontiers in endocrinology · 2021Review
- N-Octanoyl-Dopamine inhibits cytokine production in activated T-cells and diminishes MHC-class-II expression as well as adhesion molecules in IFNγ-stimulated endothelial cells.Scientific reports · 2019Article
- Article
- Decreased expression of TRPV1 in renal cell carcinoma: association with tumor Fuhrman grades and histopathological subtypes.Cancer management and research · 2018Article
- Review
- Transient receptor potential channels in the vasculature.Physiological reviews · 2015Review
- N-Octanoyl dopamine transiently inhibits T cell proliferation via G1 cell-cycle arrest and inhibition of redox-dependent transcription factors.Journal of leukocyte biology · 2014Article
- Open lung approach with low tidal volume mechanical ventilation attenuates lung injury in rats with massive brain damage.Critical care (London, England) · 2014Article
- Article
- Article
- N-octanoyl dopamine inhibits the expression of a subset of κB regulated genes: potential role of p65 Ser276 phosphorylation.PloS one · 2013Article
- Article
Corrections and comments
- Erratum issued
Authors and funding
15 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Since stimulation of transient receptor potential channels of the vanilloid receptor subtype 1 (TRPV1) mitigates acute kidney injury (AKI) and endogenous N-acyl dopamine derivatives are able to activate TRPV1, we tested if synthetic N-octanoyl-dopamine (NOD) activates TRPV1 and if it improves AKI. These properties of NOD and its intrinsic anti-inflammatory character were compared with those of dopamine (DA). TRPV1 activation and anti-inflammatory properties of NOD and DA were tested using primary cell cultures in vitro. The influence of NOD and DA on AKI was tested in a prospective, randomized, controlled animal study with 42 inbred male Lewis rats (LEW, RT1), treated intravenously with equimolar concentrations of DA or NOD one hour before the onset of warm ischemia and immediately before clamp release. NOD, but not DA, activates TRPV1 channels in isolated dorsal root ganglion neurons (DRG) that innervate several tissues including kidney. In TNFα stimulated proximal tubular epithelial cells, inhibition of NFκB and subsequent inhibition of VCAM1 expression by NOD was significantly stronger than by DA. NOD improved renal function compared to DA and saline controls. Histology revealed protective effects of NOD on tubular epithelium at day 5 and a reduced number of monocytes in renal tissue of DA and NOD treated rats. Our data demonstrate that NOD but not DA activates TRPV1 and that NOD has superior anti-inflammatory properties in vitro. Although NOD mitigates deterioration in renal function after AKI, further studies are required to assess to what extend this is causally related to TRPV1 activation and/or desensitization.
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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.