ArticleBritish journal of pharmacology2002
Role of tachykinin NK receptors on the local and remote injuries following ischaemia and reperfusion of the superior mesenteric artery in the rat.
Article in British journal of pharmacology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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14 citing papers in PubMed, 40 citations in OpenAlex.
- Protease-activated receptor 2 protects against myocardial ischemia-reperfusion injury through the lipoxygenase pathway and TRPV1 channels.Experimental and therapeutic medicine · 2019Article
- The Role of Neurogenic Inflammation in Blood-Brain Barrier Disruption and Development of Cerebral Oedema Following Acute Central Nervous System (CNS) Injury.International journal of molecular sciences · 2017Review
- Ischemia/Reperfusion.Comprehensive Physiology · 2016Review
- Neurogenic inflammation after traumatic brain injury and its potentiation of classical inflammation.Journal of neuroinflammation · 2016Review
- Biomarkers of cognitive dysfunction in traumatic brain injury.Journal of neural transmission (Vienna, Austria : 1996) · 2014Review
- Low-level laser therapy attenuates the myeloperoxidase activity and inflammatory mediator generation in lung inflammation induced by gut ischemia and reperfusion: a dose-response study.Journal of lasers in medical sciences · 2014Article
- Cell biology of ischemia/reperfusion injury.International review of cell and molecular biology · 2012Review
- Anti-inflammatory effects of limb ischaemic preconditioning are mediated by sensory nerve activation in rats.Naunyn-Schmiedeberg's archives of pharmacology · 2011Article
- Substance P antagonists as a therapeutic approach to improving outcome following traumatic brain injury.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2010Review
- APT070 (Mirococept), a membrane-localised complement inhibitor, inhibits inflammatory responses that follow intestinal ischaemia and reperfusion injury.British journal of pharmacology · 2005Article
- Ischemia-reperfusion injury of the intestine and protective strategies against injury.Digestive diseases and sciences · 2004Review
- Repertaxin, a novel inhibitor of rat CXCR2 function, inhibits inflammatory responses that follow intestinal ischaemia and reperfusion injury.British journal of pharmacology · 2004Article
- Neurokinin NK1 and NK3 receptors as targets for drugs to treat gastrointestinal motility disorders and pain.British journal of pharmacology · 2004Review
- Role of the bradykinin B2 receptor for the local and systemic inflammatory response that follows severe reperfusion injury.British journal of pharmacology · 2003Article
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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
Neuropeptides acting on tachykinin NK receptors play an important role in the amplification of inflammatory responses. We have assessed the effects of tachykinin NK receptor blockade on the injuries following intestinal ischaemia and reperfusion (I/R) in rats. The tachykinin NK(1) receptor antagonist SR140333 dose-dependently (0.05 to 0.5 mg kg(-1)) suppressed the local (intestine) and remote (lung) increases in vascular permeability and neutrophil recruitment following mild I/R injury. A structurally-distinct NK(1) receptor antagonist, CP99,994, but not tachykinin NK(2) or NK(3) receptor antagonists also suppressed mild I/R injury. Neonatal pretreatment with capsaicin effectively depleted sensory neurons and abrogated the injuries following mild I/R. Treatment with SR140333 (0.5 mg kg(-1)) significantly reversed severe reperfusion-induced local and remote increases in vascular permeability, neutrophil recruitment, intestinal haemorrhage and blood neutropaenia, but did not prevent the lethality associated with severe I/R. Post-ischaemic treatment with SR140333 significantly inhibited the elevations of TNF-alpha in the intestine and lung, but not serum, following severe I/R. The increase in the concentrations of IL-10 in the lung and serum were also suppressed. Post-ischaemic blockade of tachykinin NK(1) receptors markedly inhibited the local and remote injuries, but not lethality, following reperfusion of the SMA in rats. Neuropeptides, possibly substance P, released from sensory nerves appear to account for the activation of these tachykinin NK(1) receptors. Antagonists of the tachykinin NK(1) receptor may be useful adjuncts in the treatment of the injuries which occur following reperfusion of an ischaemic vascular territory.
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