The disappearance rate of intraventricular bradykinin in the brain of the conscious rat

Kariya, Kimio; Yamauchi, Aiko; Hattori, S.; Tsuda, Yuko; Okada, Yoshio

doi:10.1016/s0006-291x(82)80163-0

Cited by 47 publications

(13 citation statements)

References 12 publications

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“…The first step is the production of BK or kallidin at the lesion site. These are rapidly degraded by peptidases known as kininases, because the half-life of BK is reported to be Ͻ30 s in plasma (Kariya et al, 1982). The degraded BK becomes B 1 agonist and activates the B 1 receptor linked to a PTXindependent G-protein, presumably G q/11 .…”

Section: The Signal Cascade Of B 1 Receptor Activationmentioning

confidence: 99%

Bradykinin-Induced Microglial Migration Mediated by B₁-Bradykinin Receptors Depends on Ca²⁺Influx via Reverse-Mode Activity of the Na⁺/Ca²⁺Exchanger

et al. 2007

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Bradykinin (BK) is produced and acts at the site of injury and inflammation. In the CNS, migration of microglia toward the lesion site plays an important role pathologically. In the present study, we investigated the effect of BK on microglial migration. Increased motility of cultured microglia was mimicked by B 1 receptor agonists and markedly inhibited by a B 1 antagonist , but not by a B 2 receptor antagonist. BK induced chemotaxis in microglia isolated from wild-type and B 2 -knock-out mice but not from B 1 -knock-out mice. BK-induced motility was not blocked by pertussis toxin but was blocked by chelating intracellular Ca 2ϩ or by low extracellular Ca 2ϩ , implying that Ca 2ϩ influx is prerequisite. Blocking the reverse mode of Na ϩ /Ca 2ϩ exchanger (NCX) completely inhibited BK-induced migration. The involvement of NCX was further confirmed by using NCX ϩ/Ϫ mice; B 1 -agonist-induced motility and chemotaxis was decreased compared with that in NCX ϩ/ϩ mice. Activation of NCX seemed to be dependent on protein kinase C and phosphoinositide 3-kinase, and resultant activation of intermediate-conductance (IK-type) Ca 2ϩ -dependent K ϩ currents (I K(Ca) ) was activated. Despite these effects, BK did not activate microglia, as judged from OX6 staining. Using in vivo lesion models and pharmacological injection to the brain, it was shown that microglial accumulation around the lesion was also dependent on B 1 receptors and I K(Ca) . These observations support the view that BK functions as a chemoattractant by using the distinct signal pathways in the brain and, thus, attracts microglia to the lesion site in vivo.

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Section: The Signal Cascade Of B 1 Receptor Activationmentioning

confidence: 99%

Bradykinin-Induced Microglial Migration Mediated by B₁-Bradykinin Receptors Depends on Ca²⁺Influx via Reverse-Mode Activity of the Na⁺/Ca²⁺Exchanger

et al. 2007

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“…Bradykinin is one of the first mediators of inflammation produced at the site of tissue injury (Walker et al, 1995 andsee Francel, 1992;Feuerstein et al, 1997 for review) and has a half-time of only 30 sec in brain and plasma (Kariya et al, 1982). Therefore, it is most likely that bradykinin is produced within the first minutes after cryogenic injury.…”

Section: Figmentioning

confidence: 99%

Role of Bradykinin B₂Receptors in the Formation of Vasogenic Brain Edema in Rats

Plesnila

Schulz

Stoffel

et al. 2001

Journal of Neurotrauma

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Bradykinin is a mediator of brain edema acting through B2 receptors. However, it is not known if bradykinin mediates the formation of cytotoxic or vasogenic brain swelling. To investigate this question we subjected rats to a cryogenic brain lesion over the left parietal cortex, a model well known to produce predominantly vasogenic brain edema. We inhibited bradykinin B2 receptors with the recently characterized nonpeptide B2 receptor antagonist, LF 16-0687. The animals were assigned to three groups (n = 10, each) receiving 10, or 100 microg/kg/min LF 16-0687 or vehicle (0.9% NaCl). Treatment started 15 min before trauma and was continued for 24 h. Another three groups of animals (n = 10, each) received 10 microg/kg/min LF 16-0687 starting 30 or 60 min after trauma or vehicle (0.9% NaCl) for 24 h. Animals were then sacrificed and swelling and water content of the brain were determined. In the vehicle treated group the traumatized hemisphere swelled by 9.3 +/- 1.1% as compared to the untraumatized contralateral side. Pretreatment with 10 microg/kg/min LF 16-0687 decreased brain swelling significantly to 6.4 +/- 1.3% (p < 0.05). Pre-treatment with 100 microg/kg/min was found to be less effective and did not result in a significant reduction of brain swelling (7.4 + 1.3%). Treatment with LF 16-0687 for 24 h (10 microg/kg/min) started 30 or 60 min after trauma did not reduce brain water content or hemispheric swelling. These results demonstrate that brain injury-mediated bradykinin production induces vasogenic brain edema by B2 receptor stimulation. Our findings further clarify the role of bradykinin in the pathophysiology of brain edema formation and confirm the therapeutic potency of bradykinin B2 receptor inhibition.

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“…The effects of kinins in biological fluids are often very short-lived. This is probably due to the fact that the biological half-life of bradykinin administered intracerebrally in the conscious rat is about 27 seconds (Kariya et al, 1982b).…”

Section: Kininsmentioning

confidence: 99%

Kinins in the brain

Figueroa

Worthy

Bhoola

1990

Human Psychopharmacology

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The disappearance rate of intraventricular bradykinin in the brain of the conscious rat

Cited by 47 publications

References 12 publications

Bradykinin-Induced Microglial Migration Mediated by B₁-Bradykinin Receptors Depends on Ca²⁺Influx via Reverse-Mode Activity of the Na⁺/Ca²⁺Exchanger

Bradykinin-Induced Microglial Migration Mediated by B₁-Bradykinin Receptors Depends on Ca²⁺Influx via Reverse-Mode Activity of the Na⁺/Ca²⁺Exchanger

Role of Bradykinin B₂Receptors in the Formation of Vasogenic Brain Edema in Rats

Kinins in the brain

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The disappearance rate of intraventricular bradykinin in the brain of the conscious rat

Cited by 47 publications

References 12 publications

Bradykinin-Induced Microglial Migration Mediated by B1-Bradykinin Receptors Depends on Ca2+Influx via Reverse-Mode Activity of the Na+/Ca2+Exchanger

Bradykinin-Induced Microglial Migration Mediated by B1-Bradykinin Receptors Depends on Ca2+Influx via Reverse-Mode Activity of the Na+/Ca2+Exchanger

Role of Bradykinin B2Receptors in the Formation of Vasogenic Brain Edema in Rats

Kinins in the brain

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Bradykinin-Induced Microglial Migration Mediated by B₁-Bradykinin Receptors Depends on Ca²⁺Influx via Reverse-Mode Activity of the Na⁺/Ca²⁺Exchanger

Bradykinin-Induced Microglial Migration Mediated by B₁-Bradykinin Receptors Depends on Ca²⁺Influx via Reverse-Mode Activity of the Na⁺/Ca²⁺Exchanger

Role of Bradykinin B₂Receptors in the Formation of Vasogenic Brain Edema in Rats