Kinin receptors in pain and inflammation

Couture, Réjean; Harrisson, Madelaine; Vianna, Rose Mari Jacobsen; Cloutier, Frank

doi:10.1016/s0014-2999(01)01318-8

Cited by 417 publications

(357 citation statements)

References 155 publications

Supporting

Mentioning

336

Contrasting

Unclassified

Order By: Relevance

“…Since bradykinin is known to facilitate the release of substance P from rat sensory neurons in culture as well as from peripheral terminals of capsaicine-sensitive primary afferents (for a review, see Couture et al, 2001), an attempt was made to ascertain whether bradykinin could be responsible Table 1 Cough-related variables during mechanical stimulation of the tracheobronchial tree and citric acid inhalation before and ∼30 min after bilateral microinjections of 5 mM losartan (n = 7) and 1 mM lisinopril (n = 7) into the caudal NTS.…”

Section: Resultsmentioning

confidence: 99%

The cough reflex is upregulated by lisinopril microinjected into the caudal nucleus tractus solitarii of the rabbit

Cinelli

Bongianni

Pantaleo

et al. 2015

Respiratory Physiology & Neurobiology

View full text Add to dashboard Cite

a b s t r a c tWe have previously shown that cough potentiation induced by intravenous administration of the AT 1 receptor antagonist losartan is lower than that induced by the ACE inhibitor lisinopril in anesthetized and awake rabbits. Since losartan and lisinopril cross the blood-brain barrier, their central action on the cough reflex can be hypothesized. Mechanical stimulation of the tracheobronchial tree and citric acid inhalation were used to induce cough reflex responses in pentobarbital sodium-anesthetized, spontaneously breathing rabbits. Bilateral microinjections (30-50 nl) of losartan (5 mM), lisinopril (1 mM), bradykinin (0.05 mM), HOE-140 (0.2 mM, a bradykinin B 2 receptor antagonist) and CP-99,994 (1 mM, an NK 1 receptor antagonist) were performed into the caudal nucleus tractus solitarii, the predominant site of termination of cough-related afferents. Lisinopril, but not losartan increased the cough number. This effect was reverted by HOE-140 or CP-99,994. Cough potentiation was also induced by bradykinin. The results support for the first time a central protussive action of lisinopril mediated by an accumulation of bradykinin and substance P.

show abstract

Section: Resultsmentioning

confidence: 99%

The cough reflex is upregulated by lisinopril microinjected into the caudal nucleus tractus solitarii of the rabbit

Cinelli

Bongianni

Pantaleo

et al. 2015

Respiratory Physiology & Neurobiology

View full text Add to dashboard Cite

show abstract

“…Our current results, showing marked expression of bradykinin B 2 receptors in neurons (see above), may point towards a direct effect of bradykinin on neuronal survival after cerebral ischemia. This effect might have been missed previously, because neurons in culture do not express bradykinin receptors (Couture et al, 2001), thereby making studies on the role of kallikrein-kinin system on neuronal survival difficult. However, a recent report showing that overexpression of kallikrein in brain macrophages reduced programmed cell death and infarction volume after experimental stroke (Xia et al, 2004), rather favors a protective role for the kinin-kallikrein system after brain injury.…”

Section: Role Of Bradykinin B 2 Receptors For Neuronal Cell Death Aftmentioning

confidence: 99%

“…It is initiated by the activation of kallikrein that cleaves kininogen to produce the nonapeptide bradykinin. Bradykinin binds to the constitutively expressed B 2 receptor, thereby exerting various actions, for example, increase of vessel permeability, induction of pain, and vasodilatation (Couture et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

Release of Bradykinin and Expression of Kinin B₂Receptors in the Brain: Role for Cell Death and Brain Edema Formation After Focal Cerebral Ischemia in Mice

Gröger¹,

Lebesgue

Pruneau

et al. 2005

J Cereb Blood Flow Metab

126

112

View full text Add to dashboard Cite

Pharmacological studies using bradykinin B 2 receptor antagonists suggest that bradykinin, an early mediator of inflammation and the main metabolite of the kallikrein-kinin system, is involved in secondary brain damage after cerebral ischemia. However, the time-course of bradykinin production and kinin receptor expression as well as the conclusive role of bradykinin B 2 receptors for brain damage after experimental stroke have not been elucidated so far. C57/Bl6 mice were subjected to 45 mins of middle cerebral artery occlusion (MCAO) and 2, 4, 8, 24, and 48 h later brains were removed for the analysis of tissue bradykinin concentration and kinin B 2 receptor mRNA and protein expression. Brain edema, infarct volume, functional outcome, and long-term survival were assessed in WT and B 2 À/À mice 24 h or 7 days after MCAO. Tissue bradykinin was maximally increased 12 h after ischemia (three-fold), while kinin B 2 receptor mRNA upregulation peaked 24 to 48 h after MCAO (10-to 12-fold versus naïve brain tissue). Immunohistochemistry revealed that kinin B 2 receptors were constitutively and widely expressed in mouse brain, were upregulated 2 h after ischemia in cells showing signs of ischemic damage, and remained upregulated in the penumbra up to 24 h after ischemia. B 2 À/À mice had improved motor function (Po0.05), smaller infarct volumes (À38%; Po0.01), developed less brain edema (À87%; Po0.05), and survived longer (Po0.01) as compared with wild-type controls. The current results show that bradykinin is produced in the brain, kinin B 2 receptors are upregulated on dying cells, and B 2 receptors are involved in cell death and brain edema formation after experimental stroke.

show abstract

“…36% for human bradykinin receptors). In general B 2 receptors (B 2 R) are constitutively expressed in most tissues including smooth muscle (Couture et al, 2001), whereas, although B 1 expression is negligible in healthy cells its' expression is inducible, being dramatically enhanced as a result of tissue injury, infection, inflammation or anoxia (Marceau et al, 1998)..…”

Section: Introductionmentioning

confidence: 99%

Bradykinin-activated contractile signalling pathways in human myometrial cells are differentially regulated by arrestin proteins

Willets

Brighton

Windell

et al. 2015

Molecular and Cellular Endocrinology

View full text Add to dashboard Cite

Bradykinin is associated with infections and inflammation, which given the strong correlation between uterine infection and preterm labour may imply that it could play a role in this process. Therefore, we investigated bradykinin signalling, and the roles that arrestin proteins play in their regulation in human myometrial cells. Bradykinin induced rapid, transient intracellular Ca 2+ increases that were inhibited following B 2 receptor (B 2 R) antagonism.

show abstract

Kinin receptors in pain and inflammation

Cited by 417 publications

References 155 publications

The cough reflex is upregulated by lisinopril microinjected into the caudal nucleus tractus solitarii of the rabbit

The cough reflex is upregulated by lisinopril microinjected into the caudal nucleus tractus solitarii of the rabbit

Release of Bradykinin and Expression of Kinin B₂Receptors in the Brain: Role for Cell Death and Brain Edema Formation After Focal Cerebral Ischemia in Mice

Bradykinin-activated contractile signalling pathways in human myometrial cells are differentially regulated by arrestin proteins

Contact Info

Product

Resources

About

Kinin receptors in pain and inflammation

Cited by 417 publications

References 155 publications

The cough reflex is upregulated by lisinopril microinjected into the caudal nucleus tractus solitarii of the rabbit

The cough reflex is upregulated by lisinopril microinjected into the caudal nucleus tractus solitarii of the rabbit

Release of Bradykinin and Expression of Kinin B2Receptors in the Brain: Role for Cell Death and Brain Edema Formation After Focal Cerebral Ischemia in Mice

Bradykinin-activated contractile signalling pathways in human myometrial cells are differentially regulated by arrestin proteins

Contact Info

Product

Resources

About

Release of Bradykinin and Expression of Kinin B₂Receptors in the Brain: Role for Cell Death and Brain Edema Formation After Focal Cerebral Ischemia in Mice