Propranolol‐induced airway hyperreactivity in guinea‐pigs

Ney, Ursula M.

doi:10.1111/j.1476-5381.1983.tb10548.x

Cited by 58 publications

(28 citation statements)

References 19 publications

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“…In contrast, enhanced bronchoconstriction following intravenous administration of ET-1 was reported in propranolol-treated guinea-pigs (Macquin-Mavier et al, 1989;Touvay et al, 1990). Since the bronchopulmonary responses to ET-1 were not potentiated by propranolol when ET-1 was administered by aerosol (Lagente et al, 1989), it may be concluded that propranolol possesses a systemic rather than a local airway activity, which may not be related to 1.-adrenoceptor blockade (Ney et al, 1983).…”

Section: Resultsmentioning

confidence: 95%

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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Section: Resultsmentioning

confidence: 95%

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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“…Interestingly, both (-)-and 51 S. SANJAR AND OTHERS (+)isomers of propranolol cause airway hyperreactivity in the guinea-pig (Ney, 1983), which indicates an effect unrelated to adrenoceptor occupancy. This conclusion is reinforced by the present study which reveals that (± )propranolol can cause hyperreactivity when infused at doses that are insufficient to effect detectable antagonism of the spasmolytic effects of (±)isoprenaline.…”

Section: Isoprenaline-induced Airway Hyperreactivitymentioning

confidence: 99%

Increased airway reactivity in the guinea‐pig follows exposure to intravenous isoprenaline.

Sanjar¹,

Kristersson²,

Mazzoni³

et al. 1990

The Journal of Physiology

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1. Intravenous infusion of (+/‐) isoprenaline (1‐100 micrograms kg‐1 h‐1) enhanced airway responses (resistance, RL; and compliance, Cdyn) to histamine (1.0‐1.8 micrograms kg‐1) and bombesin (100‐240 ng kg‐1), whereas airway responses to vagal stimulation remained unchanged. 2. Bilateral vagotomy before intravenous infusion of (+/‐)isoprenaline (100 micrograms kg‐1 h‐1) prevented development of airway hyperreactivity to histamine or bombesin, yet vagotomy after infusion of isoprenaline was without effect. 3. Prior treatment with atropine (1 mg kg‐1) did not influence the capacity of (+/‐)isoprenaline (100 micrograms kg‐1 h‐1) to increase airway reactivity to bombesin. 4. Despite a 500‐fold difference in spasmolytic potency in vivo, infusion of (+)isoprenaline (100 micrograms kg‐1 h‐1) or (‐)isoprenaline (100 micrograms kg‐1 h‐1) increased reactivity of the airways to histamine or bombesin to a comparable extent. 5. Neither adrenaline (100 micrograms kg‐1 h‐1) nor forskolin (600 micrograms kg‐1 h‐1) increased reactivity of the airways to histamine or bombesin. 6. Intravenous infusion of dopamine (100 micrograms kg‐1 h‐1) or noradrenaline (100 micrograms kg‐1 h‐1) increased reactivity of the airways to histamine or bombesin. 7. Intravenous infusion of (+/‐) propranolol (100 micrograms kg‐1 h‐1) increased reactivity of the airways to histamine or bombesin which was partially inhibited by bilateral vagal section. 8. Depletion of circulating platelets by lytic anti‐platelet serum or concomitant infusion of an antagonist of platelet‐activating factor (PAF), ginkgolide B (1 mg kg‐1 h‐1) did not diminish the capacity of (+/‐)isoprenaline (100 micrograms kg‐1 h‐1) to induce hyperreactivity of the airways to histamine or bombesin. 9. These observations indicate that (+/‐)isoprenaline can induce airway hyper‐reactivity by a mechanism unrelated to beta‐adrenoceptor activation, but which is dependent upon intact vagus nerves.

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“…Several laboratories, including our own, have demonstrated an enhanced airway responsiveness to exogenous spasmogens or antigen after treatment with β–adrenoceptor antagonists [15, 17, 19, 27, 28]. It has been suggested that this increase in responsiveness is due to a decrease in the adrenergic tone generated by circulating catecholamines acting at β2–adrenoceptors [29, 30].…”

Section: Discussionmentioning

confidence: 99%

Food Restriction–Mediated Adrenal Influences on Antigen–Induced Bronchoconstriction and Airway Eosinophil Influx in the Guinea Pig

Underwood¹,

Matthews²,

Osborn³

et al. 1998

Int Arch Allergy Immunol

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The aim of this study was to measure the effects of food restriction on antigen–induced bronchoconstriction and inflammatory cell influx in guinea pigs and to determine the role of plasma cortisol and catecholamine concentrations. Ovalbumin (OA; 0.3 mg/kg, i.v.) was administered to OA–sensitized, anesthetized guinea pigs which had been allowed free access to food or had been food restricted for 18 h prior to OA challenge. In addition to higher plasma levels of epinephrine (30% increase) and cortisol (33% increase), fasted guinea pigs had significantly lower (60% decreased) maximal bronchoconstrictor responses to OA than nonfasted, sensitized litter mates. Additionally, groups of fasted or fed animals were subdivided into two additional treatment groups: (1) saline–pretreated or (2) polyethylene glycol 400 (PEG)–pretreated (1 ml/kg, p.o., 1 h prior to antigen challenge). In saline–treated, fasted animals, bronchoconstrictor responses to antigen were significantly diminished (67% decreased) and epinephrine and cortisol levels were increased (64 and 34%, respectively) compared to the corresponding fed group. In both fasted and fed groups, the PEG–treated guinea pigs had higher plasma epinephrine and cortisol levels than animals which received saline, but no significant differences were detected within the PEG–treated group. Plasma norepinephrine concentrations were lower in all fasted groups. In a separate model in conscious guinea pigs, there were no differences in aerosol OA–induced bronchoconstriction and eosinophil influx between fasted and fed groups. However, compared to the saline pretreatment group, PEG administration reduced the antigen–induced bronchoconstriction and eosinophilia in both fed and fasted guinea pigs. We speculate that the reduced responsiveness to antigen in fasted versus fed animals may result from food–restriction–induced, stress–related release of epinephrine and cortisol from the adrenal glands, thereby suppressing mast cell degranulation or reducing responsiveness to spasmogenic and chemotactic mediators. In addition, the results suggest that oral dosing with 100% PEG may enhance this phenomenon.

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Propranolol‐induced airway hyperreactivity in guinea‐pigs

Cited by 58 publications

References 19 publications

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

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

Increased airway reactivity in the guinea‐pig follows exposure to intravenous isoprenaline.

Food Restriction–Mediated Adrenal Influences on Antigen–Induced Bronchoconstriction and Airway Eosinophil Influx in the Guinea Pig

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