Role of the kinin‐kallikrein pathway in allergic diseases

Polosa, Riccardo

doi:10.1111/j.1398-9995.1993.tb00719.x

Cited by 22 publications

(24 citation statements)

References 74 publications

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“…20 /PC 30 FEV 1 to both methacholine and bradykinin. Subjects attended on two visits to the laboratory, at least 72 h apart, to undertake concentration-response studies with inhaled methacholine and bradykinin.…”

Section: Methodsmentioning

confidence: 99%

“…Vp 30 measurements were found to be repeatable with individual CVs ranging from 5 to 13%. 20 : provocative concentration producing a 20% fall in FEV 1 ; F: female; M: male; % pred: percentage of prediction; S: inhaled salbutamol (prn); Bf: inhaled beclomethasone (500-1,000 µg·day -1 ) .…”

Section: Measurementsmentioning

confidence: 99%

“…Although the wide array of pharmacological activities possessed by bradykinin may be relevant to inflammatory mechanisms in asthma [20], there is uncertainty about the ability of bradykinin to induce bronchial hyperresponsiveness in man and its clinical significance. As part of a series of studies evaluating the role of bradykinin in asthma, we have investigated the changes in airway calibre and in bronchial reactivity to inhaled histamine, after a single bronchoprovocative dose of bradykinin and methacholine, in a double-blind randomized study on asthmatic subjects.…”

mentioning

confidence: 99%

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Effect of inhaled bradykinin on indices of airway responsiveness in asthmatic subjects

Polosa¹,

Rajakulasingam²,

Prosperini³

et al. 1994

Eur Respir J

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E Ef ff fe ec ct t o of f i in nh ha al le ed d b br ra ad dy yk ki in ni in n o on n iin nd di ic ce es s o of f a ai ir rw wa ay y r re es sp po on ns si iv ve en ne es ss s i in n a as st th hm ma at ti ic c s su ub bj je ec ct ts s We have, therefore, investigated the effect of inhaled bradykinin on the changes in airway calibre and in airway hyperresponsiveness to histamine, in a double-blind, randomized study of nine asthmatic subjects. Subjects were studied on two study periods, separated by at least 15 days. On the first day of each study period, subjects inhaled either a single dose of bradykinin or methacholine (placebo) with changes in airway calibre being followed as forced expiratory volume in one second (FEV 1 ) and as the maximum expiratory flow rate measured at 70% of the vital capacity below total lung capacity (TLC) from a partial forced expiratory manoeuvre (Vp 30 ) Inhalation of bradykinin caused rapid bronchoconstriction that peaked at 3-5 min. When compared to placebo, no significant difference in histamine responsiveness was seen after bradykinin in terms of changes in PC 20 FEV 1 values. However, when airway hyperresponsiveness was measured as PC 40 Vp 30 , we were able to show a significant increase in airway reactivity after bradykinin at 3 and 7 h, the geometric mean PC 40 Vp 30 histamine value decreasing 3.2 and 1.9 fold, respectively.The results of the present study indicate that bradykinin elicits a transient increase of airway hyperresponsiveness in asthmatic subjects, but this was evident only using a sensitive indicator of the changes in airway reactivity, which suggests an effect at the level of the more peripheral airways. These data suggest that bradykinin may play a role in the pathogenesis of airway hyperresponsiveness in human asthma.

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Section: Methodsmentioning

confidence: 99%

Section: Measurementsmentioning

confidence: 99%

mentioning

confidence: 99%

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Effect of inhaled bradykinin on indices of airway responsiveness in asthmatic subjects

Polosa¹,

Rajakulasingam²,

Prosperini³

et al. 1994

Eur Respir J

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“…Local actions of BK and Lys-BK produce, among others, vasodilatation, increased vascular permeability, stimulation of nociceptive nerve terminals causing hyperalgesia and pain, and spasmogenic e ect on smooth muscles (Bhoola et al, 1992a;Sharma, 1993;Perkins et al, 1995;Walker et al, 1995;Poole et al, 1999;Ahluwalia & Perretti, 1999). For this reason, kinins have been involved in the pathogenesis of in¯ammatory processes like rheumatoid arthritis and asthma (Bhoola et al 1992b;Polosa, 1993;Bond et al, 1997;Deshandra & Bhoola, 1998).…”

Section: Introductionmentioning

confidence: 99%

“…In addition, the tissue kallikreindependent pathway has been involved in rheumathoid arthritis (Selwyn et al, 1989;Williams et al, 1997), allergic diseases (Polosa, 1993) and experimental pancreatitis (Blackberg & Ohlsson, 1994). Burton & Benetos (1989) and Okunishi et al (1989) reported the e ects of tissue kallikrein inhibitors in the blood pressure of the rat.…”

Section: Introductionmentioning

confidence: 99%

Evidence for activation of the tissue kallikrein‐kinin system in nociceptive transmission and inflammatory responses of mice using a specific enzyme inhibitor

Emim¹,

Souccar²,

Castro³

et al. 2000

British J Pharmacology

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1 The pharmacological activity of phenylacetyl-Phe-Ser-Arg-N-(2,4-dinitrophenyl)-ethylenediamine (TKI), a tissue kallikrein speci®c inhibitor, was assessed using models of nociception and in¯ammation in mice. 2 Injection of TKI (13.6 ± 136 mmol kg 71 , i.p. or 41 ± 410 mmol kg 71 , s.c.) produced a dose-related inhibition of the acetic acid-induced writhes (by 37 to 85% or 34 to 80%, respectively). The antinociceptive activity of TKI (41 mmol kg 71 , i.p.) was maximal after 30 min injection and lasted for 120 min. The e ect was unaltered by pretreatment with naloxone (8.2 mmol kg 71 , s.c.) or bilateral adrenalectomy. 3 TKI (41 and 136 mmol kg 71 , i.p.) produced a dose-related decrease of the late phase of formalininduced nociception by 79 and 98%, respectively. At 136 mmol kg 71 , i.p., TKI also shortened the duration of paw licking in the early phase by 69%. TKI (41 and 136 mmol kg 71 , i.p.) also reduced the capsaicin-induced nociceptive response (by 51 to 79%). 4 TKI (41 mmol kg 71 , i.p. or 410 mmol kg 71 , s.c.) reduced the oedematogenic response, from the second to the ®fth hour after carrageenin injection by 36 to 30% or by 47 to 39%, respectively. 5 Pretreatment with TKI (41 mmol kg 71 , i.p.) reduced the capsaicin-induced neurogenic in¯ammation in the mouse ear by 54%. 6 It is concluded that TKI presents antinociceptive and antiin¯ammatory activities mediated by inhibition of kinin formation by tissue kallikrein in mice. The results also indicate that the tissue kallikrein-dependent pathway contributes to kinin generation in nociceptive and in¯ammatory processes in mice.

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Pathophysiology of Viral Respiratory Tract Infections

Åkerlund¹,

Bende²

1996

Viral and Other Infections of the Human Respiratory Tract

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Role of the kinin‐kallikrein pathway in allergic diseases

Cited by 22 publications

References 74 publications

Effect of inhaled bradykinin on indices of airway responsiveness in asthmatic subjects

Effect of inhaled bradykinin on indices of airway responsiveness in asthmatic subjects

Evidence for activation of the tissue kallikrein‐kinin system in nociceptive transmission and inflammatory responses of mice using a specific enzyme inhibitor

Pathophysiology of Viral Respiratory Tract Infections

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