Vasoactive Intestinal Polypeptide Promotes Cyclic Adenosine 3‘,5’‐mono‐phosphate Accumulation in Guinea‐pig Trachea

Frandsen, Erik; Krishna, Gopal; Said, Sami I.

doi:10.1111/j.1476-5381.1978.tb08471.x

Cited by 53 publications

(20 citation statements)

References 12 publications

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“…VIP has been shown to relax guinea-pig trachea (Piper, Said & Vane, 1970;Matsuzaki et al 1980) and to increase cyclic AMP production in the same tissue (Frandsen, Krishna & Said, 1978). In the cat trachea (Ito & Takeda, 1982) VIP produced relaxation similar to the effect of inhibitory nerve stimulation, and the response to nerve stimulation was reduced by the prior application of several desensitizing doses of VIP.…”

Section: Discussionmentioning

confidence: 92%

The Quest for the Inhibitory Neurotransmitter in Bovine Tracheal Smooth Muscle

et al. 1983

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SUMMARYThe effect of inhibitory nerve stimulation on the mechanical, membrane potential and membrane conductance responses of isolated bovine tracheal smooth muscle has been studied.Membrane responses were measured in a sucrose-gap apparatus. In order to record inhibitory responses, it was necessary to increase tone in the preparation by applying a drug such as histamine. When tone was raised, repetitive field stimulation of intrinsic nerves caused depolarization and contraction, followed by relaxation and a suppression of histamine-induced slow waves. Hyperpolarization of the membrane was only seen following prolonged nerve stimulation, and there was no change in membrane conductance. The inhibitory effect of nerve stimulation was abolished by tetrodotoxin, but was not abolished by atropine, indomethacin, propranolol, naloxone or the purinergic blockers quinidine and theophylline. It was not satisfactorily mimicked by catecholamines, by y-amino-n-butyric acid (GABA) or by purines.Nerves with catecholamine fluorescence could not be found in the tracheal muscle layer. Neither adrenergic nor purinergic types of nerve terminal could be found in the tracheal muscle layer during ultrastructural examination of over one thousand nerve profiles. Vasoactive intestinal peptide (VIP) caused relaxation of the histamine-contracted tracheal muscle, suppressed the slow wave and caused slight hyperpolarization at higher concentrations, without affecting the membrane conductance. VIP was found in samples of tracheal muscle at a mean concentration of 1-95 ng/g. When the effluent solution flowing past isolated tracheal muscle strips was assayed for VIP, samples collected during inhibitory nerve stimulation had much higher concentrations ofthe peptide than samples collected before stimulation, after stimulation, or during stimulation in the presence of tetrodotoxin (10-6 mol/l). The VIP content of the effluent during control periods was 73-8 pg/ml, and during stimulation was 167 5 pg/ml. It is suggested that VIP might be the non-adrenergic inhibitory neurotransmitter in bovine tracheal smooth muscle.

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Section: Discussionmentioning

confidence: 92%

The Quest for the Inhibitory Neurotransmitter in Bovine Tracheal Smooth Muscle

et al. 1983

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“…VPAC 2 receptor mRNA levels are detected with decreasing intensity in central nervous system, heart, pancreas, skeletal muscle, kidney, lung, stomach, and liver. Robberecht et al, 1981Robberecht et al, , 1988 and by an immunocytochemical reporter for increases in intracellular cyclic AMP (Lazarus et al, 1986) that is formed when VIP stimulates adenylyl cyclase (Frandsen et al, 1978). Ligand binding sites were initially reported in airway smooth muscle of large but not small airways and in pulmonary vascular smooth muscle.…”

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confidence: 99%

Expression and Distribution of Vasoactive Intestinal Polypeptide Receptor VPAC2 mRNA in Human Airways

Groneberg

Hartmann

Dinh

et al. 2001

Laboratory Investigation

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SUMMARY:Vasoactive intestinal polypeptide (VIP) is a putative neurotransmitter of the inhibitory non-adrenergic noncholinergic nervous system and influences many aspects of mammalian airway function. VIP binds to two G-protein-coupled VPAC receptors that are highly homologous structurally but distinguished by their different affinities for peptide analogues of VIP. As VIP binding sites in the respiratory tract have only been examined by ligand binding and cytochemical techniques, we studied the distribution of the mRNA that encodes the inducible receptor subtype VPAC 2 in the human respiratory tract. Northern blots demonstrated the expression of VPAC 2 mRNA in human airways and other tissues. A human-specific VPAC 2 cRNA probe was used to detect VPAC 2 mRNA expression in human lung by nonradioactive in situ hybridization. In larger airways, positive VPAC 2 mRNA signals were localized to tracheal and bronchial ciliated epithelial cells. There was also marked staining of mucous and serous cells of submucosal glands. No signals were obtained in airway and vascular smooth muscle myocytes and endothelial cells. In peripheral lung tissues, VPAC 2 mRNA expression was localized to epithelial cells of the bronchioles. Specific staining was detected in immune cells and alveolar macrophages. In summary, VPAC 2 is localized in airway epithelial, glandular, and immune cells of the lung but not in airway and vascular smooth muscle. The absence of VPAC 2 mRNA in vascular and airway smooth muscle myocytes may indicate that the effects of VIP on vasodilation and bronchodilation are mediated by VPAC 1 or undefined receptors. However, a paracrine modulation of the two most prominent effects of VIP in the respiratory tract by VPAC 2 cannot be excluded. (Lab Invest 2001, 81:749 -755).T he 28-amino acid vasoactive intestinal polypeptide (VIP) is a putative neurotransmitter or neuromodulator of the inhibitory non-adrenergic noncholinergic nervous system in mammalian airways (Maggi et al, 1995). VIP-immunoreactivity (VIP-IR) is present in cells of the tracheobronchial smooth muscle layer, in the walls of pulmonary and bronchial vessels, around submucosal glands, in the lamina propria, and in pulmonary ganglia (Dey et al, 1981;Lundberg et al, 1984). VIP-IR nerve fibers are found as branching networks in the respiratory tract (Ghatei et al, 1982) They decrease in frequency as the airways become smaller but extend to peripheral bronchioles (Lundberg et al, 1984). The pattern of VIPergic nerves largely follows that of cholinergic nerves (Laitinen et al, 1985). VIP-IR is also present in sensory nerves (Lundberg et al, 1984;Luts and Sundler, 1989).Several studies using receptor binding techniques have been performed to demonstrate the presence of VIP receptors and have shown abundant binding in different parts of the lungs Robberecht et al, 1981Robberecht et al, , 1988. Two types of VIP receptors have been cloned and characterized in the past years. They were termed the VPAC 1 receptor, formerly described as the VIP 1 receptor (Ishihara et a...

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“…At present, at least two VIP receptors can be distinguished [81][82][83][84]. Binding of VIP to its receptors (which is dependent on its C-terminal part [85]) activates adenyl cyclase, resulting in elevated cAMP levels [86]. The effects of VIP are, therefore, often similar to the effects of ß-adrenergic receptor agonists.…”

Section: I-nanc Nervous Systemmentioning

confidence: 83%

Autonomic Innervation of Human Airways: Structure, Function, and Pathophysiology in Asthma

Velden¹,

Hulsmann

1999

Neuroimmunomodulation

129

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The human airways are innervated via efferent and afferent autonomic nerves, which regulate many aspects of airway function. It has been suggested that neural control of the airways may be abnormal in asthmatic patients, and that neurogenic mechanisms may contribute to the pathogenesis and pathophysiology of asthma. In this review, the autonomic innervation of the human airways and possible abnormalities in asthma are discussed. The parasympathetic nervous system is the dominant neuronal pathway in the control of airway smooth muscle tone. Stimulation of cholinergic nerves causes bronchoconstriction, mucus secretion, and bronchial vasodilation. Although abnormalities of the cholinergic innervation have been suggested in asthma, thus far the evidence for cholinergic dysfunction in asthmatic subjects is not convincing. Sympathetic nerves may control tracheobronchial blood vessels, but no innervation of human airway smooth muscle has been demonstrated. β-Adrenergic receptors, however, are abundantly expressed on human airway smooth muscle and activation of these receptors causes bronchodilation. The physiological role of β-adrenergic receptors is unclear and their function seems normal in asthmatic patients. Inhibitory nonadrenergic noncholinergic (NANC) nerves, containing vasoactive intestinal peptide and nitric oxide, may be the only neural bronchodilator pathways in human airways. Although a dysfunction of inhibitory NANC nerves has been proposed in asthma, thus far no differences in inhibitory NANC responses have been found between asthmatics and healthy subjects. Excitatory NANC nerves, extensively studied in animal airways, have also been detected in human airways. In animal studies, stimulation of excitatory NANC nerves causes bronchoconstriction, mucus secretion, vascular hyperpermeability, cough, and vasodilation, a process called ‘neurogenic inflammation’. Recent studies have demonstrated an interaction between the excitatory NANC nervous system and inflammatory cells. Neuropeptides may influence the recruitment, proliferation, and activation of leukocytes. On the other hand, inflammatory cells may modulate the neuronal phenotype and function. The functional relevance of the excitatory NANC nervous system and its interaction with the immune system in asthma still remains to be elucidated.

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Vasoactive Intestinal Polypeptide Promotes Cyclic Adenosine 3‘,5’‐mono‐phosphate Accumulation in Guinea‐pig Trachea

Cited by 53 publications

References 12 publications

The Quest for the Inhibitory Neurotransmitter in Bovine Tracheal Smooth Muscle

The Quest for the Inhibitory Neurotransmitter in Bovine Tracheal Smooth Muscle

Expression and Distribution of Vasoactive Intestinal Polypeptide Receptor VPAC2 mRNA in Human Airways

Autonomic Innervation of Human Airways: Structure, Function, and Pathophysiology in Asthma

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