Potentiation of the pro-inflammatory effects of bradykinin by inhibition of angiotensin-converting enzyme and aminopeptidase P in rat paws

Damas, Jacques; Liégeois, Jean-François; Simmons, William H.

doi:10.1007/bf00170844

Cited by 12 publications

(8 citation statements)

References 36 publications

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“…It was not reduced by HOE140 which is very active against other inflammatory reactions like carrageenan oedema (Wirth et al 1991;Damas and Remacle-Volon 1992). The reaction to formalin was not increased by captopril which largely enhances the effects of bradykinin and the oedemas in which bradykinin takes part (Damas et al 1996b). These results indicate a minor role of bradykinin in the vascular changes.…”

Section: Treatmentmentioning

confidence: 52%

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The inflammatory reaction induced by formalin in the rat paw

Damas

Liégeois

1999

Naunyn-Schmiedeberg's Arch Pharmacol

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The involvement of bradykinin and some other inflammatory mediators in formalin-induced oedema and plasma extravasation was examined. Formalin was injected in rat paws at two doses, 1.75% or 5%. The lower dose induced the development of an immediate oedema associated with a progressive accumulation of 125I-labelled albumin in the paws. These changes were suppressed by pretreatment with capsaicin or xylocaine. They were abolished by RP67580, a NK1 receptor antagonist, and increased by phosphoramidon or diprotin A. They were not affected by HOE140, a bradykinin B2 antagonist, captopril, methysergide, mepyramine, indomethacin, ketoprofen or L-N(G)-nitroarginine. The higher dose of formalin induced a swelling of the paws which took place in two phases associated with two periods of increase in vascular permeability. This oedema was reduced by pretreatment with capsaicin but not with xylocaine. It was reduced by RP67580 injected before or 30 min after formalin. It was inhibited by mepyramine, methysergide, indomethacin and NS-398, a cyclooxygenase-2 inhibitor. It was not modified by HOE140. Its development was similar in normal and kininogen-deficient rats. We concluded that formalin administered at a low dose induces an oedema which mainly results from a neurogenic inflammation mediated by neuropeptides such as substance P. At higher doses, formalin induces an oedema which mainly depends on the release of substance P, prostanoids, 5-hydroxytryptamine and histamine. Bradykinin plays no significant role in the vascular changes whereas this peptide has been reported to participate in the stimulation of nociceptive afferent neurons. This discrepancy could be explained by a difference in the threshold of stimulation of the nociceptive neurons and that of the cells of the vascular walls, or by a formation of kinins in close contact of the neurons.

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Section: Treatmentmentioning

confidence: 52%

“…The first one was the simultaneous injection of formalin with captopril (2×10 -4 M). This angiotensin-converting enzyme inhibitor largely increases the oedema induced by bradykinin in rat paws (Damas et al 1996b). The paws were cut 30 or 60 min after the injection of formalin alone or of formalin with captopril.…”

Section: Involvement Of Bradykininmentioning

confidence: 99%

The inflammatory reaction induced by formalin in the rat paw

Damas

Liégeois

1999

Naunyn-Schmiedeberg's Arch Pharmacol

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“…In the present study, similar levels of APP activity were detected in both the mouse lung and trachea. APP is one of the main BKmetabolizing enzymes (5) and largely contributes to the degradation of BK in several organs (11,16), especially under the inhibition of ACE activity (17). Since the increased BK exerts biological responses (microvascular leakage) in mouse tracheas after treatment with ACE inhibitors (18), we think that APP also contributes to the degradation of the increased airway BK under the conditions of ACE inhibition.…”

Section: Discussionmentioning

confidence: 99%

Different Effects of Imidapril and Enalapril on Aminopeptidase P Activity in the Mouse Trachea

et al. 2005

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“…Fucoidin was injected intravenously at a dose of 10 mg kg −1 , 15 min prior to LPS or BK. To minimise kinin degradation, 5 mg kg −1 of captopril, a kininase II inhibitor (Corrêa & Calixto, 1993; Damas et al ., 1996) was injected s.c. 1 h before BK or DABK. Aiming to examine the role of endogenous kinins in the neutrophil migration to LPS, a set of animals was pre treated with captopril before this stimulus.…”

Section: Methodsmentioning

confidence: 99%

Effect of a kinin B₂ receptor antagonist on LPS‐ and cytokine‐induced neutrophil migration in rats

Santos

Calixto

Souza

2003

British J Pharmacology

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1 This study examines the involvement of kinins in neutrophil migration into rat subcutaneous air pouches triggered by lipopolysaccharide (LPS), as well as the putative roles played by kinin B 1 and B 2 receptors, tumour necrosis factor alpha (TNF-a), interleukin-1 beta (IL-1b) and selectins in this response. 2 LPS (5 ng to 10 mg cavity À1 ) injected into the 6-day-old pouch induced a dose-and time-dependent neutrophil migration which peaked between 4 and 6 h, and was maximal following the dose of 100 ng cavity À1 (saline: 0.4670.1; LPS: 4373.70 Â 10 6 cells cavity À1 at 6 h). 3 Bradykinin (BK) (600 nmol) injected into the pouch of saline-treated rats induced only modest neutrophil migration (0.7370.16 Â 10 6 cells cavity À1 ). A more robust response to BK (3.270.25 Â 10 6 cells cavity À1 ) was seen in animals pretreated with captopril, but this was still smaller than the responses to IL-1b or TNF-a (15 pmol: 2372.2 Â 10 6 and 75 pmol: 29.572 Â 10 6 cells cavity À1 , respectively). Nevertheless, the B 1 agonist des-Arg 9 -BK (600 nmol) failed to induce neutrophil migration. 4 HOE-140 (1 and 2 mg kg À1 ), a B 2 receptor antagonist, reduced LPS-induced neutrophil migration. HOE-140 also reduced the neutrophil migration induced by BK, but had no effect on the migration promoted by IL-1b or TNF-a. des-Arg 9 -[Leu 8 ]-BK, B 1 receptor antagonist was ineffective in changing neutrophil migration caused by any of these stimuli. 5 Neutrophil migration induced by LPS or BK was reduced by interleukin-1 receptor antagonist (IL1ra) (1 mg kg À1 ), sheep anti-rat TNF serum (anti-TNF serum) (0.3 ml cavity À1 ), and the nonspecific selectin inhibitor fucoidin (10 mg kg À1 ). 6 TNF-a levels in the pouch fluid were increased by LPS or BK injection, peaking at 0.5 -1 h and gradually declining thereafter up to 6 h. IL-1b levels increased steadily throughout the 6 h period. HOE-140 markedly inhibited the rise in IL-1b and TNF-a levels in pouch fluid triggered by both stimuli. 7 These results indicate that BK participates importantly in selectin-dependent neutrophil migration into the air pouch triggered by LPS in the rat, by stimulating B 2 receptors coupled to synthesis/release of TNF-a and IL-1b.

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Potentiation of the pro-inflammatory effects of bradykinin by inhibition of angiotensin-converting enzyme and aminopeptidase P in rat paws

Abstract: The influence of some peptidase inhibitors on oedema and plasma extravasation induced by bradykinin and carrageenan in rat paw was evaluated. Bradykinin-induced oedema in normal rats was increased by o-phenanthroline (3.

Cited by 12 publications

References 36 publications

The inflammatory reaction induced by formalin in the rat paw

The inflammatory reaction induced by formalin in the rat paw

Different Effects of Imidapril and Enalapril on Aminopeptidase P Activity in the Mouse Trachea

Effect of a kinin B₂ receptor antagonist on LPS‐ and cytokine‐induced neutrophil migration in rats

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Potentiation of the pro-inflammatory effects of bradykinin by inhibition of angiotensin-converting enzyme and aminopeptidase P in rat paws

Abstract: The influence of some peptidase inhibitors on oedema and plasma extravasation induced by bradykinin and carrageenan in rat paw was evaluated. Bradykinin-induced oedema in normal rats was increased by o-phenanthroline (3.

Cited by 12 publications

References 36 publications

The inflammatory reaction induced by formalin in the rat paw

The inflammatory reaction induced by formalin in the rat paw

Different Effects of Imidapril and Enalapril on Aminopeptidase P Activity in the Mouse Trachea

Effect of a kinin B2 receptor antagonist on LPS‐ and cytokine‐induced neutrophil migration in rats

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Effect of a kinin B₂ receptor antagonist on LPS‐ and cytokine‐induced neutrophil migration in rats