Modulatory effect of neuropeptide Y on acetylcholine‐induced oedema and vasoconstriction in isolated perfused lungs of rabbit

  title={Modulatory effect of neuropeptide Y on acetylcholine‐induced oedema and vasoconstriction in isolated perfused lungs of rabbit},
  author={Annie Delaunois and Pascal Gustin and Cécile Dessy-Doizé and Michel Ansay},
  journal={British Journal of Pharmacology},
1 The modulatory role of neuropeptide Y (NPY) on pulmonary oedema induced by acetylcholine and capsaicin was investigated. The effects of NPY on the haemodynamic response to acetylcholine, phenylephrine and substance P were also investigated. 2 Isolated, ventilated, exsanguinated lungs of the rabbit were perfused with a constant flow of recirculating blood‐free perfusate. The double/arterial/venous occlusion method was used to partition the total pressure gradient (ΔPt) into four components… 

Effect of neuropeptide Y on hemodynamics of the rabbit lung.

Although NPY is a potent vasoconstrictor in the rabbit lung, it is not likely that plasma NPY concentrations rise sufficiently, even after massive sympathetic nervous system activation, to produce pulmonary vasoconStriction in the intact rabbit.

Interactions between acetylcholine and substance P effects on lung mechanics in the rabbit

It is concluded that ACh‐induced changes in lung resistance and compliance are in part mediated by a direct effect on airway smooth muscle and in part by the stimulation of C fibers, by the release of histamine from mast cells and by the synthesis of arachidonic acid metabolites.

Interactions between cytochrome P-450 activities and ozone-induced modulatory effects on endothelial permeability in rabbit lungs: influence of gender.

It was concluded that inhibition of 2 different CYP450-dependent activities after exposure to 0.4 ppm O(3) for 4 h appears to be a gender-dependent phenomenon, and that CYP 450 is probably involved in the O( 3)-evoked inhibitory mechanism against ACh-induced increase in endothelial permeability, but only in males.

Ozone-induced stimulation of pulmonary sympathetic fibers: a protective mechanism against edema.

Using a model of permeability edema in isolated perfused rabbit lungs, it is reported that, immediately after exposure of rabbits to 0.4 ppm ozone for 4 hr, the pulmonary microvascular responses to acetylcholine and substance P are completely blocked, resulting in transient protection against pulmonary edema.

Non-neuronal neuropeptide Y and its receptors during acute rejection of rat pulmonary allografts.

Role of Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) in Modulating Vascular Smooth Muscle Cells by Activating Large-Conductance Potassium Ion Channels

Evidence that the K+ channels are modulated by a direct action of non-steroidal antiinflammatory drugs (NSAIDs) to activate the K- ion channels is presented.

Comparison of ozone-induced effects on lung mechanics and hemodynamics in the rabbit.

It is concluded that O3 can induce direct vascular constriction and inhibit the ACh-, SP-, and histamine-induced changes in lung mechanical properties.



Role of neuropeptides in acetylcholine-induced edema in isolated and perfused rabbit lungs.

ACh-induced pulmonary edema was due to an increase in the capillary filtration coefficient, and 5-HT effects were prevented by aspirin and not by (+/-)-CP 96-345.

Modulation of the acetylcholine- and substance P-induced pulmonary edema by calcitonin gene-related peptide in the rabbit.

It is hypothesized that CGRP exerts a positive retro-control on the release of neuropeptides by these fibers but can attenuate their effects on the target cells.

Effects of capsaicin on the endothelial permeability in isolated and perfused rabbit lungs

It was concluded that capsaicin‐induced pulmonary oedema was due to an increase in the capillary filtration coefficient and not to hemodynamic changes.

Neuropeptide Y potentiates the effect of various vasoconstrictor agents on rabbit blood vessels

NPY (30 nM) potentiated the contractile response to noradrenaline and histamine but not to 5‐hydroxytryptamine or high K+.The response to histamine was augmented in both arteries and veins, whereas the response to noadrenalin was enhanced in arteries but not in veins.

Neuropeptide Y potentiates noradrenaline-evoked vasoconstriction: mode of action.

The potentiation of NA-evoked vasoconstriction by NPY seems to depend upon the presence of Na+ but not upon a Ca++ influx, while an intracellular sequestered Ca++ pool appears to play a critical role.

Modulation of cholinergic neurotransmission in guinea‐pig trachea by neuropeptide Y

Neuropeptide Y appears to reduce the cholinergic component to EFS via a prejunctional mechanism, acting directly on receptors onCholinergic nerve terminals, rather than affecting adrenergic mechanisms.