Circulating plasma kinin in patients with bronchial asthma

Abe, Keishi; Watanabe, Nobuhisa; Kumagai, Naoya; Mouri, Toraichi; Seki, T.; Yoshinaga, Kaoru

doi:10.1007/bf02144161

Cited by 85 publications

(28 citation statements)

References 5 publications

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“…Bradykinin may be released by inflammatory cells (Newball et al, 1979;Proud et al, 1985) whilst reduced concentrations of the bradykinin-precursor kininogen in the plasma of asthmatics coupled with raised levels of esterase enzyme activity and plasma kinins (Abe et al, 1967;Bortkiewicz, 1983) indicate a role for bradykinin in asthma. The results of the present study suggest that if bradykinin is generated in asthma its effects on plasma exudation are likely to be prolonged and contribute significantly to the airway inflammation which may underlie bronchial hyperresponsiveness (Hogg et al, 1987).…”

Section: Discussionmentioning

confidence: 99%

Bradykinin‐induced plasma exudation in guinea‐pig airways: involvement of platelet activating factor

Rogers

Dijk

Barnes

1990

British J Pharmacology

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1 We studied the effect of bradykinin on plasma exudation in the airways of the anaesthetized guineapig in vivo. Tissue content of extravasated Evans blue dye was used as an index of protein exudation in the larynx, trachea, main bronchi and intrapulmonary airways (i.p.a.). 2 Bradykinin increased the content of Evans blue in all tissues studied in a dose-related manner. The response was greatest in the main bronchi and i.p.a., less in the trachea and least in the larynx. A dose of 47 nmol kg-1 was the lowest tested which caused significant (P < 0.001) plasma exudation with increases in leakage above control values of 256% in the larynx, 405% in the trachea, 394% in the main bronchi and 485% in intrapulmonary airways. 3 Leakage was significantly (P < 0.05) increased above control values by 1 min after bradykinin (47nmol kg-1) in the main bronchi and intrapulmonary airways and was maximal in all airways 5min after bradykinin. Although reduced by 15min, the tissue content of dye was still significantly (P < 0.05) increased 2 h after bradykinin. 4 The prolonged tissue dye retention was due to a later phase of slow and maintained exudation preventing full clearance of dye after the initial response. 5The initial phase of leakage was partially attenuated by the platelet activating factor (PAF) receptor antagonists WEB 2086 or BN 52021, by indomethacin or by inhibiting sensory nerve activation by opioid anaesthesia: it was not affected by mepyramine and cimetidine nor by the sulphidopeptide leukotriene receptor antagonists FPL 55712 or ICI 198,615. Adrenoceptor blockade of the anti-leakage effects of endogenously-released catecholamines significantly (P < 0.05) enhanced leakage. 6 The later phase of plasma leakage was completely inhibited by the PAF antagonists. 7 We conclude that, in guinea-pig airways in vivo, the initial phase of bradykinin-induced plasma exudation is mediated in part by PAF, sensory nerves and prostaglandins, whereas the later, prolonged phase of leakage is mediated exclusively by PAF. If bradykinin is generated in asthma, its potent and prolonged effects on plasma leakage may contribute significantly to airway oedema and may be involved in the development of bronchial hyperresponsiveness.

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Section: Discussionmentioning

confidence: 99%

Bradykinin‐induced plasma exudation in guinea‐pig airways: involvement of platelet activating factor

Rogers

Dijk

Barnes

1990

British J Pharmacology

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“…Furthermore, asthmatic patients have an elevated kinin concentration in plasma (Abe et al, 1967) and in bronchoalveolar lavage fluid after antigen challenge (Christiansen et al, 1987).…”

Section: Introductionmentioning

confidence: 99%

The effect of peptidase inhibitors on bradykinin‐induced bronchoconstriction in guinea‐pigs in vivo

Ichinose¹,

Barnes²

1990

British J Pharmacology

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1 Bradykinin (BK) instilled directly into the airway lumen caused bronchoconstriction in anaesthetized, mechanically ventilated guinea-pigs in the presence of propranolol (1 mg kg-i.v.) The geometric mean dose of BK required to produce 100% increase in airway opening pressure (PD100) was 22.9 nmol (95% c.i. 11.7-44.6 nmol). 2 The dose-response curve for the effect of instilled BK was significantly shifted to the left by the angiotensin converting enzyme (ACE) inhibitor, captopril (5 and 50nmol instillation, PD100 = 3.0, 95% c.i. 0.98-8.9, and 2.0 nmol, 95% ci. 0.65-6.2 nmol, respectively). 3 The neutral endopeptidase (NEP) inhibitor, phosphoramidon (5 and 50nmol instillation) also shifted the dose-response curve for the effect of instilled BK; the PD100 values = 2.2 (95% c.i. 0.40-11.7) and 1.8 nmol (95% c.i. 0.87-3.5 nmol), respectively. 4 After pretreatment with captopril (50nmol) and phosphoramidon (50nmol) in combination, the doseresponse curve for the effect of instilled BK (PD100 = 1.1 nmol, 95% c.i. 0.37-3.2 nmol) was similar to that obtained in the presence of each inhibitor used alone. 5The kininase I inhibitor, DL-2-mercaptomethyl-3-guanidinoethylthiopropionic acid (50 nmol instillation) failed to alter the dose-response curve to instilled BK (PD1oo = 14.6nmol, 95% c.i. 6.7-32.0 nmol). 6 These data suggest that both ACE and NEP degrade BK in the airway lumen, but that kininase I is not involved.

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“…As it has been reported that allergens increase bronchovascular permeability in the airways of human subjects with allergic asthma [7] and that asthmatic patients have an elevated concentration of kinin in their plasma [6], it seems likely that a concentration of Bk high enough to cause bronchoconstriction may gain access to airway C-fibres by diffusing from the plasma.…”

Section: Discussionmentioning

confidence: 99%

“…In asthmatic patients, however, higher kinin concentrations have been observed in plasma and in bronchoalveolar lavage (BAL) fluid after antigen challenge [6,7]. It is also known that bradykinin causes constriction of isolated airway smooth muscle in some animal species [4,8], and also causes bronchoconstriction in asthmatic subjects when given by inhalation [9,10] or by rapid injection intravenously [11,12].…”

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confidence: 99%

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Role of tachykinins in bronchoconstriction induced by intravenous administration of bradykinin in guinea-pigs

Kuroiwa

Umeno²,

Nogami³

et al. 1996

Eur Respir J

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Total pulmonary resistance (RL) was measured using a pressure-volume sensitive body plethysmograph in anaesthetized artificially ventilated guinea-pigs pretreated with atropine (1 mg·kg -1 ) and propranolol (1 mg·kg -1 ).In the control group, i.v. administration of Bk produced a dose-dependent increase in RL. In animals pretreated with FK224, bronchoconstriction induced by higher doses of Bk (10, 50 and 100 µg·kg -1 ) was significantly reduced, whilst the bronchoconstriction caused by lower doses of Bk (5 and 7.5 µg·kg -1 ) was not. Pretreatment with a combination of FK224 and indomethacin markedly inhibited the bronchoconstriction induced by each dose of Bk compared with the groups pretreated with FK224 alone. Although pretreatment with indomethacin alone significantly reduced RL at a high dose of Bk (50 µg·kg -1 ), the reduction was significantly lower than that produced by a combination of FK224 and indomethacin.These results suggest that intravenous administration of a high dose of bradykinin causes bronchoconstriction both by cyclo-oxygenase products and by release of tachykinins.

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Circulating plasma kinin in patients with bronchial asthma

Cited by 85 publications

References 5 publications

Bradykinin‐induced plasma exudation in guinea‐pig airways: involvement of platelet activating factor

Bradykinin‐induced plasma exudation in guinea‐pig airways: involvement of platelet activating factor

The effect of peptidase inhibitors on bradykinin‐induced bronchoconstriction in guinea‐pigs in vivo

Role of tachykinins in bronchoconstriction induced by intravenous administration of bradykinin in guinea-pigs

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