Immunological Changes of Airways Smooth Muscle Reactivity

Souhrada, M.; Souhrada, J. F.

doi:10.1007/978-3-0348-7408-3_8

Cited by 3 publications

(4 citation statements)

References 88 publications

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“…By using the active sensitizing technique described by Andersson (1980), levels of both IgE and IgG should be raised in the guinea‐pig. Heating the serum from actively sensitized guinea‐pigs to inactivate IgE and not IgG, does not remove its capacity to passively sensitize guinea‐pig lung parenchymal strips in vitro (Souhrada & Souhrada, 1994). Thus, both IgE and IgG appear to be responsible for the passive sensitization.…”

Section: Discussionmentioning

confidence: 99%

Contractile responses to adenosine, R‐PIA and ovalbumen in passively sensitized guinea‐pig isolated airways

Martin

Broadley

2002

British J Pharmacology

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1 Responses to adenosine, R-PIA and ovalbumen were examined in guinea-pig isolated superfused tracheal spirals to determine the eects of passive sensitization by overnight incubation in serum from ovalbumen (OA)-sensitized or non-sensitized guinea-pigs. 2 Tissues incubated with serum from non-sensitized and OA-sensitized guinea-pigs contracted (0.07+0.02 and 0.04+0.01 g, respectively) to adenosine (300 mM) whereas non-incubated or Krebsincubated tissues produced no contractions to adenosine or ovalbumen (10 mg). Ovalbumen caused substantial contractions (0.40+0.09 g) after OA-sensitized serum incubation and signi®cantly (P50.05) smaller contractions (0.08+0.03 g) after non-sensitized serum incubation. Tracheae from guinea-pigs actively sensitized to ovalbumen 14 ± 21 days beforehand also contracted to adenosine, R-PIA (3 mM) and ovalbumen. 3 The A 1 /A 2 adenosine receptor antagonist, 8-phenyltheophylline (8-PT, 3 mM), failed to antagonize these contractions, suggesting that A 1 /A 2 adenosine receptors were not involved. 4 Unlike adenosine, R-PIA (3 mM) produced contractions in non-incubated (0.23+0.04 g) or Krebs-incubated (0.15+0.04 g) tracheae, as well as after passive and active sensitization. None of these responses were blocked by 8-PT. 5 The A 3 receptor agonist, IB-MECA, in the presence of 8-PT produced small contractions in passively sensitized tracheae (10 mM, 0.02+0.003 g) and, in larger doses (100 mM and 1 mM), contracted actively sensitized tracheae. 6 In actively sensitized trachea, the A 3 receptor antagonist, MRS-1220 (100 nM), signi®cantly (P50.05) attenuated adenosine contractions in the presence of 8-PT from 0.23+0.07 g to 0.07+0.03 g. 7 These results show that passive, like active sensitization, reveals bronchoconstrictions to adenosine of isolated tracheae. The insensitivity to 8-PT blockade, the antagonism by MRS-1220, and the fact that the A 3 receptor agonist, IB-MECA, mimics this response, suggest involvement of A 3 receptors. R-PIA, however, has a dierent pro®le of adenosine receptor activity.

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Section: Discussionmentioning

confidence: 99%

Contractile responses to adenosine, R‐PIA and ovalbumen in passively sensitized guinea‐pig isolated airways

Martin

Broadley

2002

British J Pharmacology

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“…Recent studies using such preparations have indicated possible roles of ion channels in the mechanisms underlying the pathology. For example, in canine and guinea-pig tracheal smooth muscle, ovalbumin, immunoglobulin G 1 and the proinflammatory cytokine interleukin (IL) -1β evoke membrane depolarization, which is blocked by preventing sodium influx (by removing external sodium or using amiloride) (21,22). Depolarization is followed by a marked and prolonged hyperpolarization that is sensitive to ouabain (which inhibits Na + /K + -ATPase) (21,22).…”

Section: Ion Channels and The Clinical Treatment Of Airway Disease Pomentioning

confidence: 99%

“…Depolarization is followed by a marked and prolonged hyperpolarization that is sensitive to ouabain (which inhibits Na + /K + -ATPase) (21,22). Both changes in V are blocked by certain protein kinase inhibitors (21). The mecha-nism that has been proposed to account for these observations involves increased membrane permeability to sodium (21,22).…”

Section: Ion Channels and The Clinical Treatment Of Airway Disease Pomentioning

confidence: 99%

“…Both changes in V are blocked by certain protein kinase inhibitors (21). The mecha-nism that has been proposed to account for these observations involves increased membrane permeability to sodium (21,22). The resultant influx of sodium ions produces three effects, the first of which is a transient membrane depolarization.…”

Section: Ion Channels and The Clinical Treatment Of Airway Disease Pomentioning

confidence: 99%

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Membrane Currents in Airway Smooth Muscle: Mechanisms and Therapeutic Implications

Janssen

1997

Canadian Respiratory Journal

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I n airway smooth muscle (ASM), the physiologically relevant end-point is contraction, leading to a decrease in airway calibre and thereby an increase in resistance to airflow. Contraction is generally accepted to be calcium-dependent, requiring an elevation of cytosolic levels of calcium ions. One mechanism by which intracellular calcium ([Ca 2+ ]i) is elevated involves influx of calcium ions through voltage-dependent calcium channels; the membrane depolarization that triggers calcium channel opening is in turn a result of changes in the activity of other ion channels. In SCIENCE OF ASTHMA LJ JANSSEN. Membrane currents in airway smooth muscle: Mechanisms and therapeutic implications. Can Respir J 1997;4(1):13-20.Electrophysiological and pharmacological techniques were used to characterize the membrane conductance changes underlying spasmogen-evoked depolarization in airway smooth muscle (ASM). Changes included a transient activation of chloride ion channels and prolonged suppression of potassium ion channels; both changes are triggered by release of internally sequestered calcium ion and in turn cause opening of voltage-dependent calcium channels. The resultant influx of calcium ions contributes to contraction as well as to refilling of the internal calcium ion pool. Bronchodilators, on the other hand, act in part through activation of potassium channels, with consequent closure of calcium channels. The tools used to study ion channels in ASM are described, and the investigations of the roles of ion channels in ASM physiology (autacoid-evoked depolarization and hyperpolarization) and pathophysiology (airway hyperresponsiveness) are summarized. Finally, how the relationship between ion channels and ASM function/dysfunction may relate to the treatment of asthma and related breathing disorders is discussed.

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Na+/K+ ATPase mediates rhythmic spontaneous relaxations in canine airway smooth muscle

Janssen

Nana

1997

Respiration Physiology

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Immunological Changes of Airways Smooth Muscle Reactivity

Cited by 3 publications

References 88 publications

Contractile responses to adenosine, R‐PIA and ovalbumen in passively sensitized guinea‐pig isolated airways

Contractile responses to adenosine, R‐PIA and ovalbumen in passively sensitized guinea‐pig isolated airways

Membrane Currents in Airway Smooth Muscle: Mechanisms and Therapeutic Implications

Na+/K+ ATPase mediates rhythmic spontaneous relaxations in canine airway smooth muscle

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