Expression of B1 and B2 bradykinin receptor mRNA and their functional roles in sympathetic ganglia and sensory dorsal root ganglia neurones from wild-type and B2 receptor knockout mice
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Cited by (79)
Commentary on Chemical transmission of nerve impulses by Zénon M. Bacq
2022, Discoveries in Pharmacology - Volume 1 - Nervous system and hormonesNerve growth factor derivative NGF61/100 promotes outgrowth of primary sensory neurons with reduced signs of nociceptive sensitization
2017, NeuropharmacologyCitation Excerpt :We found that HOE-140 significantly reduced SP release induced by BK both in control NGF61 and NGF61/100 treated cultures (Fig. 4C), demonstrating that BK induces SP release by a selective interaction with B2 receptors in both NGF61/100 and control NGF61 treated cultures. The BK receptor B2R is expressed in sensory neurons (Petersen et al., 1998; Seabrook et al., 1997) where its expression is up-regulated by NGF (Lee et al., 2002). Since in NGF61/100-treated DRG BK stimulation evokes a reduced release of SP and CGRP, as compared to control NGF61, we wondered whether this difference could be ascribed to a different B2R expression in the two cultures.
Protein kinase C enhances human sodium channel hNav1.7 resurgent currents via a serine residue in the domain III-IV linker
2014, FEBS LettersCitation Excerpt :We recently showed that a group of inflammatory mediators including PGE2, Bradykinin, ATP, histamine, and serotonin can increase resurgent currents in DRG neurons [20]. Several of these inflammatory mediators can activate the PKC pathway, either directly or indirectly [17,27]. The current finding of PKC increasing resurgent currents of hNav1.7 in HEK293 cells suggest that PKC activation might contribute to the effects of inflammatory mediators on resurgent currents in DRG neurons.
Effects of Bradykinin on Nociceptors
2009, NeuroImmune BiologyCitation Excerpt :In uninflamed tissues, most effects of bradykinin are mediated by B2 receptors as shown by studies employing selective peptide (HOE 140 also known as icatibant, NPC 18521) and nonpeptide B2 receptor antagonists (WIN 64338, FR 173657, NPC 18884, and bradyzide) as well as B2 receptor knock-out mice [22–49]. Consistent with this, selective B1 receptor agonists do not activate or sensitize nociceptors under normal conditions [14,22,24,26,30,31,35, 41–43,48,50–59]. Although B1 receptors are generally considered not to participate in the acute effects of bradykinin, some studies provided evidence against this.