The role of Autocoids and TRPV1 in mediation of Neurogenic inflammation
The role of Inflammatory autacoids,bradykinin and PGE2, & their intracellular signalling pathways in the induction of hyperalgesia
Versandkostenfrei!
Versandfertig in 6-10 Tagen
32,99 €
inkl. MwSt.
PAYBACK Punkte
16 °P sammeln!
In this study we have investigated the sensitising effect that Prostaglandin E2 (PGE2) has on the action of bradykinin (BK) in both depolarising the resting membrane potential and in action potential generation and propagation in the isolated, desheathed vagus nerve using an extra cellular grease gap recording technique. Prostaglandin E2 sensitisation of the bradykinin induced depolarisation is mimicked by both activation of the protein kinase A and protein kinase C signalling pathways by a process that is completely blocked by the TRPV1 antagonist ruthenium red and staurosporin. This suggests...
In this study we have investigated the sensitising effect that Prostaglandin E2 (PGE2) has on the action of bradykinin (BK) in both depolarising the resting membrane potential and in action potential generation and propagation in the isolated, desheathed vagus nerve using an extra cellular grease gap recording technique. Prostaglandin E2 sensitisation of the bradykinin induced depolarisation is mimicked by both activation of the protein kinase A and protein kinase C signalling pathways by a process that is completely blocked by the TRPV1 antagonist ruthenium red and staurosporin. This suggests a pivotal role for the vanilloid capsaicin sensitive receptor TRPV1 channel in the prostaglandin E2 and bradykinin induced response.
Andere Kunden interessierten sich für
