The Action of Sodium Cromoglycate on ‘C’ Fibre Endings in the Dog Lung

Dixon, M; Jackson, D.M.; Richards, Ivan M.

doi:10.1111/j.1476-5381.1980.tb10898.x

Cited by 187 publications

(71 citation statements)

References 11 publications

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“…Moreover, pharmacological evidence suggests that tachykinins could participate in the pathogenesis of airflow obstruction induced by isocapnic dry gas hyperpnoea in human subjects with asthma. Indeed, sodium cromoglycate which inhibits C-fibres discharge (Dixon et al, 1980) and thus the release of tachykinins or the tachykinin receptor antagonist, SCH 37224 (Solway & Leff, 1991) blunt hyperpnoea-induced broncho-obstruction in asthma. Similarly, it has been suggested that VIP and related peptides released from airway cholinergic nerves may also play a role in asthma (Barnes, 1989).…”

Section: Introductionmentioning

confidence: 99%

Effect of passive sensitization on the mechanical activity of human isolated bronchial smooth muscle induced by substance P, neurokinin A and VIP

Ben‐Jebria

Marthan

Rossetti

et al. 1993

British J Pharmacology

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1 The effect of passive sensitization on the mechanical activity of human isolated bronchial smooth muscle induced by the following neuropeptides substance P (SP), neurokinin A (NKA) and vasoactive intestinal peptide (VIP) was studied both in the absence and in the presence of the neutral endopeptidase (NEP) inhibitor, phosphoramidon. 2 Cumulative concentration-response curves (CCRC) to these neuropeptides were constructed in human passively sensitized isolated bronchial rings and compared to those in paired controls. Passively sensitized human isolated bronchial rings were tissues incubated overnight in serum from asthmatic patients atopic to Dermatophagoides pteronyssinus and paired controls were tissues originating from the same lung specimens but incubated overnight in serum from healthy donors. 3 In the absence of phosphoramidon, passive sensitization significantly increased the amplitude of the contractile responses to SP and NKA including that to the maximal concentration given from 50 ± 5% to 76 + 6% (n = 5, P<0.05) and from 70 ± 7% to 101 ± 6% (n = 5, P<0.05) of the maximal response to acetylcholine, respectively. Passive sensitization significantly shifted to the left the CCRC for both tachykinins as measured by the geometric means dose-ratios which were 8.5 (95% confidence limits (CL): 3.1-13.9) and 7.3 (95% CL: 4.2-10.3) for SP and NKA, respectively. 4 In the presence of phosphoramidon (10 gM), passive sensitization still increased significantly the amplitude of the contractile responses to SP and NKA including that to the maximal concentration given from 74 ± 4% to 115 + 7% (n = 5, P<0.05) and from 104 ± 9% to 146 + 16% (n = 5, P<0.05) of the maximal response to acetylcholine, respectively. Passive sensitization still significantly shifted to the left the CCRC for both tachykinins as measured by the dose-ratios which were 9.0 (95% CL: 4.3-13.6) and 5.4 (95% CL: 2.9-7.9) for SP and NKA, respectively. 5 The relaxant response to the maximal concentration of VIP given in tissues precontracted with histamine (0.5 mM) was significantly reduced by passive sensitization from 41 ± 4% to 25 + 3% (n = 5, P <0.05) of the amplitude of the precontraction in the absence of phosphoramidon and from 72 + 1% to 49 ± 4% (n = 5, P<0.05) in the presence of phosphoramidon (10 4M). Passive sensitization significantly shifted to the right the CCRC for VIP as measured by the dose-ratios which were 10.4 (95% CL: 6.6-14.1) and 6.4 (95% CL: 3.0-9.8) in the absence and in the presence of phosphoramidon, respectively. 6 We conclude that passive sensitization enhances the mechanical response to neuropeptides which contract human isolated bronchial smooth muscle and reduces that to a neuropeptide which relaxes it. The mechanism of passive sensitization-induced changes in the mechanical activity appears to be independent of a decrease in NEP activity since these changes persist in the presence of the NEP inhibitor, phosphoramidon.

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Section: Introductionmentioning

confidence: 99%

Effect of passive sensitization on the mechanical activity of human isolated bronchial smooth muscle induced by substance P, neurokinin A and VIP

Ben‐Jebria

Marthan

Rossetti

et al. 1993

British J Pharmacology

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“…In addition, the response to methoxamine was not observed in the absence of atropine, in which case bronchoconstrictor responses may well have been greater. The dose of ipratropium bromide used in the present study is sufficient to block a standard methacholine challenge (Woolcock et cold air (Breslin et al, 1980) SO2 (Harries et al, 1981) and hypotonic nebulized solutions in man (Fuller & Collier, 1984) and that following stimulation of reflex arcs in dogs (Dixon et al, 1980 (Tattersfield, 1981). There was no significant difference between the mean values for FEV, after the three pretreatments.…”

Section: Discussionmentioning

confidence: 63%

Inhibition of methoxamine‐induced bronchoconstriction by ipratropium bromide and disodium cromoglycate in asthmatic subjects.

Black¹,

Vincenc²,

Salome³

1985

Brit J Clinical Pharma

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We compared the effects of pretreatment with saline, ipratropium bromide, and disodium cromoglycate (DSCG) on bronchoconstriction induced by methoxamine‐an alpha‐adrenoceptor agonist, in asthmatic subjects. All 12 patients bronchoconstricted in response to methoxamine after saline. The PD20 (the dose of methoxamine causing a 20% fall in forced expiratory volume in 1 s [FEV1]) ranged from 0.3‐18 mumol. Ipratropium bromide (200 micrograms administered by aerosol) significantly inhibited (P less than 0.05) the response to methoxamine in all patients without producing significant changes in the mean baseline lung function. The mean PD20 for methoxamine after saline was 6.8 mumol and 95% confidence limits (CL) were 3.6, 12.7 mumol. The mean PD20 for methoxamine after ipratropium bromide was 35.4 (95% CL 28.8, 43.6) mumol. DSCG also produced significant (P less than 0.05) shifts to the right in the methoxamine dose response curves, but did not affect resting airway calibre as measured by the FEV1. The mean PD20 for methoxamine increased from 3.3 mumol (95% CL 1.1, 10.0 mumol) after saline to 25.1 mumol (95% CL 14.1, 44.6) after DSCG pretreatment. These findings suggest that alpha‐adrenoceptors in the airways of asthmatic subjects may be located at sites other than smooth muscle‐possibly on mast cells but more likely on nerve endings and/or parasympathetic ganglia.

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“…Sodium cromoglycate inhibits unmyelinated afferent vagal pathways in dogs (Dixon et al, 1980) and in some species bradykinin causes bronchoconstriction by activation of C-fibre sensory nerve endings (Kaufman et al, 1980). This suggests that sodium cromoglycate and nedocromil sodium may inhibit sensory activation by bradykinin.…”

Section: Discussionmentioning

confidence: 94%

Bradykinin‐induced bronchoconstriction: inhibition by nedocromil sodium and sodium cromoglycate.

Dixon

Barnes

1989

Brit J Clinical Pharma

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1 The effects of inhaled nedocromil sodium and sodium cromoglycate on bradykinininduced bronchoconstriction have been studied in a double-blind, placebo controlled study, in eight mild asthmatic subjects. 2 The subjects attended on four occasions. Fifteen minutes after drug pre-treatment a bradykinin challenge was performed. Increasing concentrations were inhaled until a greater than 40% fall in expiratory flow at 30% of vital capacity from a partial flow volume manoeuvre (Vp30) was demonstrated.3 Inhaled bradykinin (0.06-8.0 mg ml-1) caused dose-related bronchoconstriction with the geometric mean cumulative dose causing a 40% fall in Vp3o (PD40) of 0.035 (95% CI: 0.02-0.07) ,umol, after placebo inhalation, which was similar to that measured before the trial (0.04: 0.02-0.09 ,umol). 4 Both nedocromil sodium (4 mg) and sodium cromoglycate (10 mg) gave significant protection (P < 0.05) against bradykinin-induced bronchoconstriction (PD40 0.37: 0.19-0.72 p,mol after nedocromil sodium and 0.22: 0.11-0.49 after sodium cromoglycate). 5 Since bradykinin-induced bronchoconstriction is probably neurally mediated we conclude that both nedocromil sodium and sodium cromoglycate have an action on neural pathways which may be useful in the control of asthma symptoms.

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The Action of Sodium Cromoglycate on ‘C’ Fibre Endings in the Dog Lung

Cited by 187 publications

References 11 publications

Effect of passive sensitization on the mechanical activity of human isolated bronchial smooth muscle induced by substance P, neurokinin A and VIP

Effect of passive sensitization on the mechanical activity of human isolated bronchial smooth muscle induced by substance P, neurokinin A and VIP

Inhibition of methoxamine‐induced bronchoconstriction by ipratropium bromide and disodium cromoglycate in asthmatic subjects.

Bradykinin‐induced bronchoconstriction: inhibition by nedocromil sodium and sodium cromoglycate.

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