Substance P: The Relationship between Receptor Distribution in Rat Lung and the Capacity of Substance P to Stimulate Vascular Permeability

Sertl, K; Wiedermann, C J; Kowalski, Marek L.; Hurtado, Sandra; Plutchok, J.; Linnoila, Ilona; Pert, Candace B.; Kaliner, M. A.

doi:10.1164/ajrccm/138.1.151

Cited by 60 publications

(18 citation statements)

References 4 publications

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“…Pretreatment with CP-96,345 inhibited poly-L-lysine-induced plasma protein extravasation throughout the airways, the exception being in the distal airways where no inhibition was observed. Such results are consistent with the lack of substance P immunoreactive nerves in the lower respiratory tract of rats (33). Similarly, tachykinin depletion has been demonstrated to inhibit increased vascular leakage induced by a variety of mediators and inflammatory stimuli including bradykinin, smoke, ozone, and formaldehyde (34).…”

Section: Discussionsupporting

confidence: 77%

Cationic protein-induced sensory nerve activation: role of substance P in airway hyperresponsiveness and plasma protein extravasation.

Coyle¹,

Perretti²,

Manzini³

et al. 1994

J. Clin. Invest.

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We have previously reported that human eosinophil granule major basic protein and synthetic cationic proteins such as poly-L-arginine and poly-L-lysine, can increase airway responsiveness in vivo. In the present study, we have investigated whether activation of sensory C-fibers is important in this phenomenon. Dose-response curves to methacholine were constructed before and 1 h after intratracheal instillation of poly-L-lysine in anaesthetized spontaneously breathing rats, and the concentration of methacholine required to induce a doubling in total lung resistance was calculated. Poly-L-lysine induced a fivefold increase in airway responsiveness, which was inhibited by neonatal capsaicin treatment and potentiated by phosphoramidon (100 jtg/ml). Furthermore, pretreatment with either CP, 96-345, or RP-67580 two selective NK-1 receptor antagonists inhibited poly-L-lysine-induced airway hyperresponsiveness and plasma protein extravasation. In vitro, cationic proteins stimulated the release of calcitonin gene-related peptidelike immunoreactivity from perfused slices of the main bronchi. Our results demonstrate that cationic proteins can activate sensory C-fibers in the airways, an effect which is important in the subsequent development of airway hyperresponsiveness and plasma protein extravasation. Cationic proteins may therefore function as a link between inflammatory cell accumulation and sensory nerve activation. (J.

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Section: Discussionsupporting

confidence: 77%

Cationic protein-induced sensory nerve activation: role of substance P in airway hyperresponsiveness and plasma protein extravasation.

Coyle¹,

Perretti²,

Manzini³

et al. 1994

J. Clin. Invest.

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“…Neuropeptides failed to contract rat isolated trachea, but mediated an epitheliumdependent, cyclo-oxygenase-sensitive relaxation of contracted rat trachea (Frossard & Muller, 1986;Devillier et al, 1992). This is consistent with the localization of substance P binding sites to airway epithelium and blood vessels in the rat (Sertl et al, 1988). In contrast, bronchoconstriction induced by intravenous administration of sensory neuropeptides, including, neurokinin A and substance P, in the rat was dependent on the release of acetylcholine from parasympathetic nerves and/or mast cell degranulation (Joos et al, 1988).…”

Section: Discussionsupporting

confidence: 83%

Poly‐l‐arginine‐mediated release of acetylcholine from parasympathetic nerves in rat and guinea‐pig airways

Spina

Goldie

1994

British J Pharmacology

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1 The synthetic cationic polypeptide, poly-L-arginine (0.03-1 mg ml-') induced concentrationdependent contraction of guinea-pig and rat isolated trachea. In guinea-pig isolated trachea, this response was attenuated in the presence of the muscarinic cholinoceptor antagonist, atropine (0.1 gM) and augmented by the acetylcholinesterase inhibitor, ecothiophate (0.1 M). The neuronal sodium channel blocker, tetrodotoxin (3 .M) failed to alter the contractile response to poly-L-arginine and acetylcholine. 2 The contractile response to poly-L-arginine in rat isolated trachea was inhibited in the presence of atropine (0.1 ILM) and the 5-hydroxytryptamine (5-HT) receptor antagonist, methysergide (1 g.M). Treatment of rat tracheal preparations with capsaicin (1 00 M) or tetrodotoxin (3 gM) failed to alter the contractile response to poly-L-arginine. In contrast, ecothiophate (0.1 JLM) augmented the contractile response to poly-L-arginine in rat isolated trachea. 3 Electrical field stimulation (5 Hz, 2 min) of epithelium-denuded guinea-pig tracheal preparations preloaded with [3H]-choline resulted in a contractile response and the simultaneous efflux of radioactivity into the superfusate. Both these responses were abolished in the presence of tetrodotoxin (L.5 gM).Poly-L-arginine (1 mg ml-') also increased the efflux of total radioactivity from epithelium-denuded guinea-pig isolated tracheal preparations preloaded with [3H]-choline, but this response was tetrodotoxin-insensitive. The negatively charged polyanion, heparin (1 mg ml-') failed to increase significantly the efflux of radioactivity from epithelium-denuded preparations. 4 In conclusion, the synthetic cationic polypeptide, poly-L-arginine, caused contraction of guinea-pig isolated tracheal preparations via the release of acetylcholine from parasympathetic nerves. Similarly, poly-L-arginine-induced contraction of rat isolated trachea is secondary to the release of acetylcholine from parasympathetic nerves and/or the release of mast cell-derived 5-HT.

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“…In the same way, substance P has a potent pulmonary vasodilatator effect when vascular tone is elevated as in the fetus (3,31). In the lung, substance P also causes mast cell degranulation and histamine release, inducing a vasodilatator response (43). Bradykinin is released during the two phases of the formalin test and may modulate pulmonary vascular tone (9,45).…”

Section: Discussionmentioning

confidence: 99%

Effects of nociceptive stimuli on the pulmonary circulation in the ovine fetus

Houfflin‐Debarge¹,

Delelis²,

Jaillard³

et al. 2005

American Journal of Physiology-Regulatory, Integrative and Comp

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The fetus is able to exhibit a stress response to painful events, and stress hormones have been shown to modulate pulmonary vascular tone. At birth, the increased level of stress hormones plays a significant role in the adaptation to postnatal life. We therefore hypothesized that pain may alter pulmonary circulation in the perinatal period. The hemodynamic response to subcutaneous injection of formalin, which is used in experimental studies as nociceptive stimulus, was evaluated in chronically prepared, fetal lambs. Fetal lambs were operated on at 128 days gestation. Catheters were placed into the ascending aorta, superior vena cava, and main pulmonary artery. An ultrasonic flow transducer was placed around the left pulmonary artery. Three subcutaneous catheters were placed in the lambs' limb. The hemodynamic responses to subcutaneous injection of formalin, to formalin after fetal analgesia by sufentanil, and to sufentanil alone were recorded. Cortisol and catecholamine concentrations were also measured. Pulmonary vascular resistances (PVR) increased by 42% (P Ͻ 0.0001) after formalin injection. Cortisol increased by 54% (P ϭ 0.05). During sufentanil infusion, PVR did not change significantly after formalin. Cortisol increased by 56% (P Ͻ 0.05). PVR did not change during sufentanil infusion. Norepinephrine levels did not change during any of the protocols. Our results indicate that nociceptive stimuli may increase the pulmonary vascular tone. This response is not mediated by an increase in circulating catecholamine levels. Analgesia prevents this effect. We speculate that this pulmonary vascular response to nociceptive stimulation may explain some hypoxemic events observed in newborn infants during painful intensive care procedures. experimental pain animal model; fetal pain; fetal analgesia; pulmonary vascular reactivity; stress hormones THE DEVELOPMENT OF FETAL INVASIVE procedures and a better knowledge about pain in preterm and full-term newborn infants have led to increased interest in the subject of fetal pain. Nociception during early development is poorly understood. However, numerous indirect evidence such as behavioral or neurohormonal responses to invasive procedures suggests that the fetus can feel pain very early in gestation (17,18,20). Fetal brain-sparing response has been observed after procedures involving transgression of fetal trunk from as early as 16 wk (54). Furthermore, transfusion through the intrahepatic veins is associated with substantial rises in stress hormones (norepinephrine, cortisol, ␤-endorphin) from as early as 18 wk of gestation (17,18).At birth, the increase in stress hormones plays a significant role in the adaptation to postnatal life, including increased left ventricular contractility, lung fluid reabsorption, and surfactant release (11,25,35,47,49,60). Stress hormones have also been shown to modulate the pulmonary vascular tone and reactivity during the perinatal life (12,26,29). These data suggest that perinatal stress may alter the pulmonary circulation. Furthermore, hyp...

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Substance P: The Relationship between Receptor Distribution in Rat Lung and the Capacity of Substance P to Stimulate Vascular Permeability

Cited by 60 publications

References 4 publications

Cationic protein-induced sensory nerve activation: role of substance P in airway hyperresponsiveness and plasma protein extravasation.

Cationic protein-induced sensory nerve activation: role of substance P in airway hyperresponsiveness and plasma protein extravasation.

Poly‐l‐arginine‐mediated release of acetylcholine from parasympathetic nerves in rat and guinea‐pig airways

Effects of nociceptive stimuli on the pulmonary circulation in the ovine fetus

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