Effects of bradykinin receptor agonists, and captopril and thiorphan in ferret isolated trachea: evidence for bradykinin generation in vitro

Farmer, Stephen G.; Broom, Terasa; DeSiato, Mark A.

doi:10.1016/0014-2999(94)90659-9

Cited by 13 publications

(5 citation statements)

References 9 publications

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“…It is possible that the BK-dependent Ca 2ϩ differences were determined at the receptor level, for example, by variations in receptor/isoform expression. In ASM cells, pharmacological and Scatchard analyses showed only a single B 2 receptor binding site (2,12). Western blot analysis did not show any differences in B 2 receptor expression between the two rat strains, indicating that the Ca 2ϩ differences between Fischer and Lewis arose downstream from the receptor.…”

Section: Discussionmentioning

confidence: 88%

Enhanced calcium signaling to bradykinin in airway smooth muscle from hyperresponsive inbred rats

Tao

Shah

Pradhan

et al. 2003

American Journal of Physiology-Lung Cellular and Molecular Phys

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Inbred Fischer 344 rats display airway hyperresponsiveness (AHR) in vivo compared with the normoresponsive Lewis strain. Fischer AHR has been linked with increased airway smooth muscle (ASM) contraction ex vivo and enhanced ASM cell intracellular Ca(2+) mobilization in response to serotonin compared with Lewis. To determine the generality of this association, we tested whether bradykinin (BK) also stimulates greater contraction of Fischer airways and greater Ca(2+) mobilization in Fischer ASM cells. Explants of Fischer intraparenchymal airways constricted faster and to a greater degree in response to BK than Lewis airways. BK also evoked higher Ca(2+) transients in Fischer than in Lewis ASM cells. ASM cell B(2) receptor expression was similar between the two strains. BK activated both phosphatidylinositide-specific phospholipase C (PI-PLC) and phosphatidylcholine-specific PLC to mobilize Ca(2+) in Fischer and Lewis ASM cells. PI-PLC activity, as measured by inositol polyphosphate accumulation, was similar in the two strains. PKC inhibition with GF109203X, Go6973, or Go6983 attenuated BK-mediated Ca(2+) transients in Fischer cells, whereas GF109203X potentiated while Go6976 and Go6983 did not affect Ca(2+) transients in Lewis cells. Enhanced Ca(2+) mobilization in ASM cells can arise from variations in PKC and may be an important component of nonspecific, innate AHR.

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Section: Discussionmentioning

confidence: 88%

Enhanced calcium signaling to bradykinin in airway smooth muscle from hyperresponsive inbred rats

Tao

Shah

Pradhan

et al. 2003

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…Bradykinin has different effects on airway smooth muscle in different species. It has rather weak or no effect on cat, dog, rabbit and rat airways, but causes contraction in ferret isolated trachea (Collier, 1963; Farmer, 1991; Farmer et al , 1994). In addition to documenting species variability, the study of pharmacology of murine tissue is increasingly interesting and important because mice are often used in transgenic and knock out studies.…”

Section: Introductionmentioning

confidence: 99%

Involvement of bradykinin B₁ and B₂ receptors in relaxation of mouse isolated trachea

Vaali

Paakkari

et al. 1998

British J Pharmacology

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1 The aim of the present study was to investigate the e ects of bradykinin and [des-Arg 9 ]-bradykinin and their relaxant mechanisms in the mouse isolated trachea. 2 In the resting tracheal preparations with intact epithelium, bradykinin and [des-Arg 9 ]-bradykinin (each drug, 0.01 ± 10 mM) induced neither contraction nor relaxation. In contrast, bradykinin (0.01 ± 10 mM) induced concentration-dependent relaxation when the tracheal preparations were precontracted with methacholine (1 mM). 5 Prostaglandin E 2 (PGE 2 , 0.01 ± 33 mM) caused concentration-dependent relaxation of the tracheal preparations precontracted with methacholine. Indomethacin (1 mM) and ODQ (10 mM) exerted no inhibitory e ects on the relaxation induced by PGE 2 . 6 The NO-donor, sodium nitroprusside (SNP; 0.01 ± 100 mM) also caused concentration-dependent relaxation of the tracheal preparations precontracted with methacholine. ODQ (0.1 ± 1 mM) concentration-dependently inhibited the relaxation induced by SNP. 7 These data demonstrate that bradykinin and [des-Arg 9 ]-bradykinin relax the mouse trachea precontracted with methacholine by the activation of bradykinin B 2 -receptors and B 1 -receptors, respectively. The stimulation of bradykinin receptors induces activation of the cyclo-oxygenase pathway, leading to the production of relaxing prostaglandins. The NO pathway is not involved in the bradykinininduced relaxation. The relaxation caused by NO-donors in the mouse trachea is likely to be mediated via activation of soluble guanylate cyclase.

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“…However, an association between ACE inhibition and kinin-dependent "proinflammatory" effects has been reported in only two instances so far: (1) in rat trachea, the combination of captopril with the NEP inhibitor phosphoramidon was reported to increase plasma extravasation, 21 and (2) pretreatment with captopril and another NEP inhibitor, thiorphan, caused a contraction in approximately 70% of ferret isolated tracheal strips, and this effect was abolished by different B 2 receptor antagonists. 22 Kinins are the obvious candidate for mediating the plasma protein vascular leakage caused by captopril in the mouse airways and digestive tract. To determine the role of kinins in the plasma extravasation induced by captopril, we used two strategies.…”

Section: Evans Blue Extravasation In Various Mouse Tissuesmentioning

confidence: 99%

Acute ACE Inhibition Causes Plasma Extravasation in Mice That is Mediated by Bradykinin and Substance P

et al. 1998

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Abstract-The use of angiotensin-converting enzyme (ACE) has been associated with the occurrence of adverse effects, including cough and angioneurotic edema. Accumulation of kinins has been suggested to play a major role in these adverse effects of ACE inhibitor, although conclusive evidence for such a role is lacking. We investigated whether ACE inhibition increases plasma extravasation in mice (Swiss, C57Bl/6J, and J129Sv/Ev strains) via inhibition of bradykinin metabolism and stimulation of neurogenic inflammatory mechanisms. Intravenous captopril and enalapril increased the extravasation of Evans blue dye in all tissues examined (trachea, stomach, duodenum, and pancreas

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Effects of bradykinin receptor agonists, and captopril and thiorphan in ferret isolated trachea: evidence for bradykinin generation in vitro

Cited by 13 publications

References 9 publications

Enhanced calcium signaling to bradykinin in airway smooth muscle from hyperresponsive inbred rats

Enhanced calcium signaling to bradykinin in airway smooth muscle from hyperresponsive inbred rats

Involvement of bradykinin B₁ and B₂ receptors in relaxation of mouse isolated trachea

Acute ACE Inhibition Causes Plasma Extravasation in Mice That is Mediated by Bradykinin and Substance P

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Effects of bradykinin receptor agonists, and captopril and thiorphan in ferret isolated trachea: evidence for bradykinin generation in vitro

Cited by 13 publications

References 9 publications

Enhanced calcium signaling to bradykinin in airway smooth muscle from hyperresponsive inbred rats

Enhanced calcium signaling to bradykinin in airway smooth muscle from hyperresponsive inbred rats

Involvement of bradykinin B1 and B2 receptors in relaxation of mouse isolated trachea

Acute ACE Inhibition Causes Plasma Extravasation in Mice That is Mediated by Bradykinin and Substance P

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Involvement of bradykinin B₁ and B₂ receptors in relaxation of mouse isolated trachea