Vasoactive Intestinal Peptide Causes Bronchodilatation and Protects Against Histamine-Induced Bronchoconstriction in Asthmatic Subjects

Morice, AH; Unwin, RJ; Sever, PS

doi:10.1016/s0140-6736(83)91272-2

Cited by 99 publications

(33 citation statements)

References 7 publications

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“…The role of endogenous VIP in the human airway, however, has not yet been investigated. In addition, the effects of VIP delivered as an aerosol in human asthmatics was less favorable than expected from animal experiments [1,18].…”

Section: Discussionmentioning

confidence: 78%

VIP antagonists enhance excitatory cholinergic neurotransmission in the human airway

Aizawa

Inoue

Shigyo

et al. 1994

Lung

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It has been reported that a low concentration of exogenously applied vasoactive intestinal peptide (VIP) suppresses the release of acetylcholine (ACh) from vagus nerve terminals in the ferret and feline trachea. There has been, however, no documentation of the prejunctional action of VIP in the human airway. We observed the effects of VIP and VIP antagonists on cholinergic excitatory neuro-effector transmission in the human bronchus to study the possible role of endogenous VIP on excitatory neurotransmission. In the human bronchus, VIP (10(-10) to 10(-7) M) showed no effect on either the contractions evoked by electrical field stimulation (EPS) or those evoked by ACh. To investigate the possible role of endogenous VIP on the human bronchus, we observed the effects of the VIP antagonists [4-Cl-D-Phe6,Leu17]-VIP and [Ac-Tyr1,D-Phe2]-GRF(1-29)-NH2 on excitatory neuro-effector transmission. Both VIP antagonists (10(-8) M) significantly enhances the contractions evoked by EFS without affecting the ACh sensitivity of smooth muscle cells. These results indicate that VIP antagonists have a prejunctional action that enhances excitatory neurotransmission. This study suggests that endogenous VIP may suppresses ACh release from the vagus nerve terminals in the human airway. It is also suggested that exogenously applied VIP may be inactivated by some mechanism in the human airway.

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Section: Discussionmentioning

confidence: 78%

VIP antagonists enhance excitatory cholinergic neurotransmission in the human airway

Aizawa

Inoue

Shigyo

et al. 1994

Lung

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“…In previous studies, the application of VIP therapy in asthmatic patients has been attempted (Morice et al, 1983;Barnes and Dixon, 1984). However, the effect of VIP has been questioned for some reasons.…”

Section: Discussionmentioning

confidence: 99%

“…Therefore, for the clinical application of VIP as a therapeutic agent, a metabolically stable analogue of VIP needs to be developed. In addition to the stability issue, there is the probability that systemic administration of VIP causes cardiovascular side effect (Morice et al, 1983), therefore the effective drug delivery system also should be applied for the specific delivery of VIP to the target tissue. Actually, the development of several drug delivery system for VIP has been attempted and they include nasal route (Dufes et al, 2003) and vector-mediated delivery (Bickel et al, 1993).…”

Section: Introductionmentioning

confidence: 99%

Development of dry powder inhalation system of novel vasoactive intestinal peptide (VIP) analogue for pulmonary administration

et al. 2006

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“…(Morice et al, 1983). Healthy, non-atopic subjects were investigated in order to minimise day to day variation in response and to reduce any effect of bronchodilation on lung mechanics during measurement of ventilatory responses.…”

Section: Plasma Catecholaminesmentioning

confidence: 99%

A comparison of the ventilatory, cardiovascular and metabolic effects of salbutamol, aminophylline and vasoactive intestinal peptide in normal subjects.

Morice¹,

Schofield²,

Keal³

et al. 1986

Brit J Clinical Pharma

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1 Intravenous infusion of placebo for 30 min followed by either salbutamol 10 ,ug min-1, aminophylline 0.2 mg kg-1 mint1 or vasoactive intestinal peptide (VIP) 6 pmol kg-' minfor 30 min was performed in a single blind fashion in six normal volunteers. 2 Both salbutamol and aminophylline increased minute ventilation, (P < 0.05) the mean increase being 26% and 19% respectively. Aminophylline also increased the ventilatory response to carbon dioxide by 47% (P < 0.05) when measured by hyperoxic rebreathing, whereas salbutamol and VIP were without significant effect. 3 All three drugs caused a tachycardia, mean increase in the pulse being 16, 8 and 2 beats min-' for salbutamol, aminophylline and VIP respectively, and aminophylline also increased both systolic and diastolic blood pressure, mean arterial pressure increasing by 14 mmHg. 4 VIP caused haemoconcentration and salbutamol the expected changes in plasma biochemistry. Plasma catecholamines increased slightly during drug infusion, although this effect is unlikely to be important.

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Vasoactive Intestinal Peptide Causes Bronchodilatation and Protects Against Histamine-Induced Bronchoconstriction in Asthmatic Subjects

Cited by 99 publications

References 7 publications

VIP antagonists enhance excitatory cholinergic neurotransmission in the human airway

VIP antagonists enhance excitatory cholinergic neurotransmission in the human airway

Development of dry powder inhalation system of novel vasoactive intestinal peptide (VIP) analogue for pulmonary administration

A comparison of the ventilatory, cardiovascular and metabolic effects of salbutamol, aminophylline and vasoactive intestinal peptide in normal subjects.

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