Vasoactive Intestinal Peptide: A Possible Transmitter of Nonadrenergic Relaxation of Guinea Pig Airways

Matsuzaki, Yoshio; Hamasaki, Yuhei; Said, Sami I.

doi:10.1126/science.6254154

Cited by 252 publications

(107 citation statements)

References 26 publications

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“…There is evidence supporting the existence of non-adrenergic, non-cholinergic (NANC) neurogenic regulation ofairway, (Matsuzaki et al, 1980;Cameron et al, 1983) genito-urinary (Snedden & Westfall, 1984 and cardiac smooth muscle (Saito et al, 1986) and NANC relaxation of coronary (Rooke et al, 1982) and other vessels (Duckles, 1979;Hamasaki et al, 1983) has been demonstrated. However, the identity of the neurotransmitters in this third nervous system are still uncertain.…”

Section: Discussionmentioning

confidence: 99%

Calcitonin gene‐related peptide (CGRP) is a potent non‐endothelium‐dependent inhibitor of coronary vasomotor tone

Greenberg

Rhoden

Barnes

1987

British J Pharmacology

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1 Ring segments of bovine left circumflex coronary artery were pre-contracted with 5-hydroxytryptamine or phenylephrine and then exposed to increasing concentrations of calcitonin gene-related peptide (CGRP) and other drugs. 2 CGRP administration resulted in dose-dependent inhibition of induced tone. Maximal relaxation to CGRP was 89 ± 5% and the concentration required to achieve 50% maximal relaxation (EC.) was 2.11 ± 1.35 x 10-9M. 3 CGRP-induced relaxation was not affected by removal of endothelial cells nor was it significantly altered by incubation of coronary vessels with atropine, propranolol, phentolamine (all 10-6 M) or indomethacin (10-5M). 4 From these data we conclude that CGRP is a potent inhibitor of coronary artery vasomotor tone which appears to act directly on vascular smooth muscle rather than through the release of a secondary mediator. These data support the possibility that CGRP may play a role in non-adrenergic, noncholinergic regulation of coronary artery tone.

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Section: Discussionmentioning

confidence: 99%

Calcitonin gene‐related peptide (CGRP) is a potent non‐endothelium‐dependent inhibitor of coronary vasomotor tone

Greenberg

Rhoden

Barnes

1987

British J Pharmacology

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“…pig (Matsuzaki et al, 1980) airway smooth muscle, a putative candidate is vasoactive intestinal peptide (VIP).…”

Section: Introductionmentioning

confidence: 99%

Effects of peptidases on non‐adrenergic, non‐cholinergic inhibitory responses of tracheal smooth muscle: a comparison with effects on VIP‐ and PHI‐induced relaxation

Ellis

Farmer

1989

British J Pharmacology

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1 The effects of peptidase enzymes on non-adrenergic, non-cholinergic (NANC) inhibitory responses of guinea-pig trachea to electrical field stimulation (EFS), and on relaxations induced by vasoactive intestinal peptide (VIP) and peptide histidine isoleucine (PHI) have been examined. 2 a-Chymotrypsin reduced both the magnitude and, particularly, the duration of the inhibitory response to EFS, whereas papain reduced only the magnitude. Aprotinin, a peptidase inhibitor prevented the effects of a-chymotrypsin but was without effect on papain. 3 a-Chymotrypsin and papain both abolished relaxant responses to exogenous VIP and PHI. The action of a-chymotrypsin was prevented by aprotinin, whereas that of papain was not affected. 4 The peptidases were without effect on concentration-response curves to methacholine or to isoprenaline. It was also observed that, in the absence of the peptidases, aprotinin had no effect on inhibitory responses either to EFS or to exogenous VIP and PHI. 5 It is suggested that neuropeptides, possibly VIP and PHI, released during EFS of guinea-pig trachea, partly mediate NANC relaxations, and that their action may be inhibited by peptidases. However, the lack of effect of aprotonin alone, on responses to EFS, suggests that, if endogenous peptidases are important in terminating the action of neuropeptides, they are resistant to the effect of this particular peptidase inhibitor. It is further suggested that neurogenic relaxation of guinea-pig trachea is also partly mediated by a substance, possibly non-peptide, other than VIP or PHI.

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“…In the presence of cholinergic and sympathetic blockade, stimulation of vagal nerves, either by electrical current or via neural reflex pathways, elicits relaxation of preconstricted ASM cells via activation of iNANC pathways (2,12,17,56). Recent studies indicate that the iNANC system employs vasoactive intestinal peptide (VIP) (7,16,22,38,47,57), nitric oxide (NO) (4,30,36,44,51), or both (6, 14 -16, 64) to elicit ASM relaxation. However, the preganglionic origin of neurons containing these relaxing molecules has not been established.…”

mentioning

confidence: 99%

“…central nervous system control of the airways; parasympathetic preganglionic neurons; choline acetyl transferase; vasoactive intestinal peptide; nitric oxide synthase; nucleus ambiguus; airway constriction; airway dilation IN MANY SPECIES, INCLUDING HUMANS, airway smooth muscle (ASM) tone critically relies on the balance between central excitatory cholinergic control (3,19,33,49) and the inhibitory nonadrenergic, noncholinergic (iNANC) influences (2,12,17,47,56). Activation of cholinergic preganglionic neurons produces airway constriction, submucosal gland secretion and increased blood flow using acetylcholine as a neurotransmitter (23,25,26).…”

mentioning

confidence: 99%

Chemical profile of vagal preganglionic motor cells innervating the airways in ferrets: the absence of noncholinergic neurons

Mayer

Haxhiu

2004

Journal of Applied Physiology

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Kc, Prabha, Catherine A. Mayer, and Musa A. Haxhiu. Chemical profile of vagal preganglionic motor cells innervating the airways in ferrets: the absence of noncholinergic neurons. J Appl Physiol 97: 1508 -1517, 2004; 10.1152/japplphysiol.00282.2004.-In ferrets, we investigated the presence of choline acetyltransferase (ChAT), vasoactive intestinal peptide (VIP), and markers for nitric oxide synthase (NOS) in preganglionic parasympathetic neurons innervating extrathoracic trachea and intrapulmonary airways. Cholera toxin ␤-subunit, a retrograde axonal transganglionic tracer, was used to identify airway-related vagal preganglionic neurons. Double-labeling immunohistochemistry and confocal microscopy were employed to characterize the chemical nature of identified airway-related vagal preganglionic neurons at a single cell level. Physiological experiments were performed to determine whether activation of the VIP and ChAT coexpressing vagal preganglionic neurons plays a role in relaxation of precontracted airway smooth muscle tone after muscarinic receptor blockade. The results showed that 1) all identified vagal preganglionic neurons innervating extrathoracic and intrapulmonary airways are acetylcholine-producing cells, 2) cholinergic neurons innervating the airways coexpress ChAT and VIP but do not contain NOS, and 3) chemical stimulation of the rostral nucleus ambiguus had no significant effect on precontracted airway smooth muscle tone after muscarinic receptor blockade. These studies indicate that vagal preganglionic neurons are cholinergic in nature and coexpress VIP but do not contain NOS; their stimulation increases cholinergic outflow, without activation of inhibitory nonadrenergic, noncholinergic ganglionic neurons, stimulation of which induces airway smooth muscle relaxation. Furthermore, these studies do not support the possibility of direct inhibitory innervation of airway smooth muscle by vagal preganglionic fibers that contain VIP.central nervous system control of the airways; parasympathetic preganglionic neurons; choline acetyl transferase; vasoactive intestinal peptide; nitric oxide synthase; nucleus ambiguus; airway constriction; airway dilation IN MANY SPECIES, INCLUDING HUMANS, airway smooth muscle (ASM) tone critically relies on the balance between central excitatory cholinergic control (3,19,33,49) and the inhibitory nonadrenergic, noncholinergic (iNANC) influences (2,12,17,47,56). Activation of cholinergic preganglionic neurons produces airway constriction, submucosal gland secretion and increased blood flow using acetylcholine as a neurotransmitter (23,25,26). In the presence of cholinergic and sympathetic blockade, stimulation of vagal nerves, either by electrical current or via neural reflex pathways, elicits relaxation of preconstricted ASM cells via activation of iNANC pathways (2,12,17,56). Recent studies indicate that the iNANC system employs vasoactive intestinal peptide (VIP) (7,16,22,38,47,57), nitric oxide (NO) (4, 30, 36, 44, 51), or both (6, 14 -16, 64) to elicit ASM relaxation. Ho...

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Vasoactive Intestinal Peptide: A Possible Transmitter of Nonadrenergic Relaxation of Guinea Pig Airways

Cited by 252 publications

References 26 publications

Calcitonin gene‐related peptide (CGRP) is a potent non‐endothelium‐dependent inhibitor of coronary vasomotor tone

Calcitonin gene‐related peptide (CGRP) is a potent non‐endothelium‐dependent inhibitor of coronary vasomotor tone

Effects of peptidases on non‐adrenergic, non‐cholinergic inhibitory responses of tracheal smooth muscle: a comparison with effects on VIP‐ and PHI‐induced relaxation

Chemical profile of vagal preganglionic motor cells innervating the airways in ferrets: the absence of noncholinergic neurons

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