Contractile activity of three endothelins (ET‐1, ET‐2 and ET‐3) on the human isolated bronchus

Advenier, C.; Sarriá, Benjamı́n; Naline, Emmanuel; Puybasset, Louis; Lagente, Vincent

doi:10.1111/j.1476-5381.1990.tb12071.x

Cited by 117 publications

(53 citation statements)

References 27 publications

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“…Acetylcholine and histamine showed a very similar contractile profile without any significant differences in Emax or pD2. The results are consistent with the results of ADVENIER et al [26] in bronchi with a diameter of 3-5 mm. The buffer solution with a high potassium concentration showed contractions which were only 53% of the acetylcholineinduced contraction.…”

Section: Discussionsupporting

confidence: 83%

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Contractile endothelin-B (ETB) receptors in human small bronchi

Adner

Cardell²,

Sjöberg

et al. 1996

Eur Respir J

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C Co on nt tr ra ac ct ti il le e e en nd do ot th he el li in n--B B ( (E ETTBIn the present paper, improved methodology was used which enables in vitro studies of small human bronchi down to a diameter of 0.5-1.0 mm. Using the new methodology we have tried to further characterize this receptor.Small bronchi from the distal parts of the bronchial tree were obtained from pulmonary tissue removed from 15 patients with lung cancer. They were dissected and cut into ring segments, in which isometric tension was recorded.ET-1, ET-2 and ET-3 elicited strong concentration-dependent contractions of the human small bronchus. Basically, the three peptides were equipotent with about the same maximal response. Upon reapplication, they all showed the same tachyphylaxis pattern, reaching half the initial contraction. Comparative analysis of IRL 1620, a selective ETB receptor agonist, revealed that the effect of the ETB agonist was, in all respects, similar to the responses induced by the ETs. PD 145065, a combined ETA/ETB receptor antagonist competitively inhibited the contractions induced by IRL 1620, whereas FR139317, a selective ETA receptor antagonist, was without effect.In conclusion, the present study shows that accurate measurements can be made in vitro on small human bronchi and all present data are in favour of an ETB receptor mediating endothelin-induced contraction of human bronchi smaller than 1.0 mm.

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Section: Discussionsupporting

confidence: 83%

“…Earlier investigations have shown that ETs are potent and strong contractors of human bronchi [16,26,27]. These studies were performed on large bronchi with a diameter of 3-15 mm.…”

Section: Discussionmentioning

confidence: 99%

Contractile endothelin-B (ETB) receptors in human small bronchi

Adner

Cardell²,

Sjöberg

et al. 1996

Eur Respir J

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“…Alternatively, it is possible that it is the putative ETc receptor (Martin et al, 1990;Samson et al, 1990;Masakai et al, 1992). However, this appears unlikely as this receptor exhibits selectivity for ET-3, whereas ET-1, ET-2 and ET-3 all have been shown to contract human bronchus with a rank order for potency and efficacy of: ET-l > ET-2 = ET-3 (Advenier et al, 1990;Hemsen et al, 1990).…”

Section: Discussionmentioning

confidence: 99%

Endothelin receptor subtypes in human and guinea‐pig pulmonary tissues

Hay

Luttmann

Hubbard

et al. 1993

British J Pharmacology

110

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1 In this study the endothelin (ET) receptor subtypes mediating contractions produced by ET-1 in human and guinea-pig pulmonary tissues were investigated. In addition the receptor responsible for ET-1-induced prostanoid release in human bronchus was determined.2 In human bronchus and human pulmonary artery ET-l (0.1 nM-0.3 JIM) was a potent and effective contractile agent (pD2 = 7.58 + 0.15, n = 6, and 8.48 + 0.11, n = 7, respectively). BQ-123 (1-10 JiM), a potent and selective ETA receptor antagonist, potently antagonized ET-1-induced contraction in human pulmonary artery (pKB = 6.8 with 1 JIM BQ-123, n = 7) but had no effect in human bronchus (n = 6). 3 Sarafotoxin S6c (0.1 nM-0. IliM), the ETB-selective agonist, did not contract human pulmonary artery (n = 5), but potently and effectively contracted human bronchus: pD2 = 8.41 ± 0.17, maximum response =74.4 ± 3.1% of 1O JM carbachol; n = 5. BQ-123 (1-1 I1M) did not antagonize sarafotoxin S6c-induced contraction in human bronchus (n = 5). 4 ET-1 potently contracted guinea-pig trachea, bronchus, pulmonary artery and aorta (pD2 = 8.15 + 0.14, 7.72 + 0.12, 8.52 + 0.12, and 8.18 ± 0.12, respectively, n = 6-14). BQ-123 (0.1-101M) antagonized ET-1-induced contractions in guinea-pig pulmonary artery (pKB = 6.7 with 1 JIM BQ-123, n = 6), aorta (pKB = 7.1 with 1 JIM BQ-123, n = 6) and trachea (pKB = 6.2 with 1 AIM BQ-123, n = 6) but was without marked effect in bronchus (n = 4). In contrast, sarafotoxin S6c (0.1 nM-0.l JIM) did not contract guinea-pig aorta (n = 4) or guinea-pig pulmonary artery (n = 6) but potently and effectively contracted guinea-pig bronchus: pD2= 8.55 + 0. 1; maximum contraction = 63.6 ± 3.1% of 1O JIM carbachol, n = 4. Sarafotoxin S6c (0.1 nM-0. 1 JIM) was a much less effective agonist in guinea-pig trachea: maximum contraction = 13.9 ± 2.5% of 10 JM carbachol, n = 4; P < 0.0001, compared to bronchus. Contractions produced by sarafotoxin S6c in guinea-pig bronchus or trachea were unaffected by (IO IM, n=4). 5 Significant differences were observed in the efficacy, relative to carbachol, but not the potency of sarafotoxin S6c in guinea-pig airways, with a much greater maximum contractile response in bronchus (69.6 ± 2.4% of 1O JM carbachol, n = 6) or lower region of the trachea (48.5 ± 5.9% of 1OJIM carbachol, n = 6) than in the middle region of the trachea (14.4 ± 4.0% of 10 JiM carbachol, n = 6) or the upper region of the trachea (19.3 ± 2.7% of 1O JM carbachol, n = 6). There were minimal regional differences in either ET-1-induced contraction or the potency of BQ-123 (3 JIM) for inhibition of responses to ET-1 in guinea-pig airways. 6 Release of various prostanoids in human bronchus induced by ET-1 (0.3 JiM) was essentially abolished with 10 IM These data provide evidence that distinct ET receptors mediate ET-1-induced contraction in human pulmonary artery, guinea-pig pulmonary artery and guinea-pig aorta (ETA subtype) compared with human bronchus and guinea-pig bronchus (non-ETA, perhaps ETB subtype). Contractions to ET-1 in guinea-pig trache...

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“…Its production in the vicinity of airway smooth muscle suggests that ET-1 could affect adjacent local airway tone. In vitro and in vivo studies indicate that ET-1 exerts a potent contractile effect on guinea-pig and human isolated bronchial and tracheal tissues (Uchida et al, 1988;Maggi et al, 1989;Borges et al, 1989;Advenier et al, 1990;Battistini et al, 1990). Furthermore, intravenous or aerosol administration of ET-1 to anaesthetized guinea-pigs evoked sustained bronchoconstriction (Payne & Whittle, 1988;Lagente et al, 1989;MacquinMavier et al, 1989).…”

Section: Introductionmentioning

confidence: 99%

Pharmacological modulation of endothelin‐induced contraction of guinea‐pig isolated airways and thromboxane release

Filep

Battistini

Sirois

1991

British J Pharmacology

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1The aim of the present experiments was to study the possible involvement of known bronchoconstrictor substances in mediating the myotropic action of endothelin-l (ET-1, human-porcine endothelin) in guinea-pig isolated airways. 2 ET-1 (1-100nm) caused a dose-dependent contraction of guinea-pig trachea, upper bronchus and parenchyma. The contractions developed slowly, reaching maximal values 4-6 min after addition of the peptide. 3 The contractile action of ET-1 was significantly attenuated by indomethacin (10uM), a cyclo-oxygenase blocker, BM 13505 (5,UM), a thromboxane receptor antagonist, FPL 55712 (19 pM) and YM 16638 (1pM), antagonists of the sulphidopeptide leukotrienes, BN 52021 (10pM) and WEB 2086 (1 pM), plateletactivating factor receptor antagonists in all three tissue preparations studied.4 Pretreatment of the airway tissues with compound U 75302 (3 guM), a selective leukotriene B4 receptor antagonist, or with a mixture of antagonists containing methysergide (0.75,UM), phentolamine (0.4UM), propranolol (13juM), atropine (0.4 pM) and diphenhydramine (0.45 pM) did not modify the myotropic action of ET-1. 5 ET-1, 10 and lOOnM induced three, and nine fold increases in thromboxane A2 release from lung parenchymal strips. 6 ET-1-induced thromboxane A2 release was completely abolished by indomethacin, and was significantly attenuated by BN 52021, WEB 2086 and FPL 55712. Neither BM 13505 nor YM 16638 exerted a significant effect on thromboxane release. 7 The present findings show that contraction of guinea-pig airway smooth muscle by ET-1 is mediated, in part, by the release of thromboxane A2, sulphidopeptide leukotrienes and platelet-activating factor, and suggest that the increased thromboxane A2 release following ET-1 is partly a consequence of enhanced synthesis of sulphidopeptide leukotrienes and platelet-activating factor.

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Contractile activity of three endothelins (ET‐1, ET‐2 and ET‐3) on the human isolated bronchus

Cited by 117 publications

References 27 publications

Contractile endothelin-B (ETB) receptors in human small bronchi

Contractile endothelin-B (ETB) receptors in human small bronchi

Endothelin receptor subtypes in human and guinea‐pig pulmonary tissues

Pharmacological modulation of endothelin‐induced contraction of guinea‐pig isolated airways and thromboxane release

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