ArticleBritish journal of pharmacology2005
TRPV1 activation results in disruption of the blood-brain barrier in the rat.
Article in British journal of pharmacology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 53 citations in OpenAlex.
- Transient receptor potential vanilloid 1 inhibition reduces brain damage by suppressing neuronal apoptosis after intracerebral hemorrhage.Brain pathology (Zurich, Switzerland) · 2024Article
- Identification of an Intravenous Injectable NK1 Receptor Antagonist for Use in Traumatic Brain Injury.International journal of molecular sciences · 2024Article
- The role of endothelial TRP channels in age-related vascular cognitive impairment and dementia.Frontiers in aging neuroscience · 2023Review
- Transient Receptor Potential Vanilloid in the Brain Gliovascular Unit: Prospective Targets in Therapy.Pharmaceutics · 2021Review
- (Neuro) Peptides, Physical Activity, and Cognition.Journal of clinical medicine · 2020Review
- Targeting the endocannabinoid system: a predictive, preventive, and personalized medicine-directed approach to the management of brain pathologies.The EPMA journal · 2020Review
- Molecular and Functional Study of Transient Receptor Potential Vanilloid 1-4 at the Rat and Human Blood-Brain Barrier Reveals Interspecies Differences.Frontiers in cell and developmental biology · 2020Article
- Innervation is higher above Bone Remodeling Surfaces and in Cortical Pores in Human Bone: Lessons from patients with primary hyperparathyroidism.Scientific reports · 2019Article
- The Influence of Capsaicin on the Integrity of Microvascular Endothelial Cell Monolayers.International journal of molecular sciences · 2018Article
- Asthma predisposition and respiratory syncytial virus infection modulate transient receptor potential vanilloid 1 function in children's airways.The Journal of allergy and clinical immunology · 2018Article
- The Role of Substance P in Secondary Pathophysiology after Traumatic Brain Injury.Frontiers in neurology · 2017Review
- Endocannabinoids: A Promising Impact for Traumatic Brain Injury.Frontiers in pharmacology · 2017Review
- Neurogenic inflammation after traumatic brain injury and its potentiation of classical inflammation.Journal of neuroinflammation · 2016Review
- Dihydrocapsaicin-induced hypothermia after asphyxiai cardiac arrest in rats.Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE Engineering in Medicine and Biology Society. Annual International Conference · 2016Article
- TREK-king the blood-brain-barrier.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2014Review
- TRPV1 gates tissue access and sustains pathogenicity in autoimmune encephalitis.Molecular medicine (Cambridge, Mass.) · 2013Article
- The role of substance p in ischaemic brain injury.Brain sciences · 2013Article
- Blocking neurogenic inflammation for the treatment of acute disorders of the central nervous system.International journal of inflammation · 2013Article
- Acute NADPH oxidase activation potentiates cerebrovascular permeability response to bradykinin in ischemia-reperfusion.Free radical biology & medicine · 2011Article
- Vascular permeability modulation at the cell, microvessel, or whole organ level: towards closing gaps in our knowledge.Cardiovascular research · 2010Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We have examined the role of TRPV1 activation in disrupting the blood-brain barrier by measuring the permeability of single pial venular capillaries in anaesthetized rats. Capsaicin application to the brain surface resulted in increased permeability, maximal 2.1+/-0.12 x 10(-6) cm s(-1) (mean+/-s.e.m.) with log EC50 -4.5+/-0.10. Substance P methyl ester gave a similar response (maximal 2.0+/-0.07, n = 6, log EC50 -4.8+/-0.07), but the selective NK2 agonist, beta-Ala8-NKA(4-10) peptide, had no effect. Although CGRP decreased the permeability of venules (log EC50 10.3+/-0.11), its receptor antagonist CGRP(8-37) had no effect on the response to capsaicin. The TRPV1 antagonist capsazepine (1 mM) reduced the response to capsaicin (100 microM), from 1.78+/-0.15 to 0.63+/-0.10 (n = 4). The NK1 receptor antagonists GR205171 (100 microM) and SDZ NKT 376 (1 mM) also reduced the response to capsaicin (from 1.75+/-0.14 to 0.46+/-0.08; n = 6, and from 1.85+/-0.13 to 0.48+/-0.05; n = 5, respectively), indicating that capsaicin acts via TRPV1 in series with NK(1). Starch microspheres were used to produce transient focal ischaemia. Permeability was increased on reperfusion to a greater extent and more rapidly in vessels with diameter greater than 40 microm than those less than 15 microm. Capsazepine given intraperitoneally during ischaemia reduced the permeability increase in small venules from 5.9+/-0.3 to 2.4+/-0.1, and from 11.4+/-0.8 to 5.1+/-0.9 in large venules. In conclusion, the TRPV1 receptor is active in the brain microvasculature and has its permeability-increasing effect via substance P. It also plays a role in the immediate blood-brain barrier disruption following ischaemia-reperfusion.
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