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  • Mast cells  (2)
  • 5-Hydroxytryptamine  (1)
  • Acetylcholine  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 322 (1983), S. 153-157 
    ISSN: 1432-1912
    Keywords: Histamine release ; Mast cells ; Substance P ; Substance P analogues ; VIP ; Somatostain ; Capsaicin ; Plasma extravasation ; Rat hindquarter preparation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 1. The release of histamine and serotonin by neuropeptides and capsaicin was measured in the isolated perfused rat hindquarter preparation. 2. Substance P and two antagonistic peptides, [d-Pro2, d-Phe7, d-Trp9]-SP and [d-Pro2, d-Trp7,9]-SP, released histamine, the SP(4-11) and SP(6-11) analogues did not. VIP and somatostatin released histamine and also serotonin. No amines were released by bombesin. Thus, all amine releasing peptides possessed at least two basic charges. However, the histamine releasing activity of the neuropeptides tested did not correlate with their reported ability to cause vasodilatation and plasma extravasation. 3. The SP(4-11) and SP(6-11) analogues which did not release histamine caused plasma extravasation. It is concluded that SP causes plasma extravasation by a direct action on blood vessels. 4. Capsaicin released only serotonin but no histamine either in untreated rats and such densensitized with capsaicin as neonates. 5. In rats desensitized with capsaicin 4 days prior to the experiment the substance P induced histamine release was as high as in untreated controls; it was, however, absent in rats desensitized with capsaicin as neonates. It is assumed that the sensitivity of mast cells to substance P is lost after degeneration of substance P containing primary sensory fibers.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 317 (1981), S. 67-70 
    ISSN: 1432-1912
    Keywords: Substance P ; Histamine ; 5-Hydroxytryptamine ; Mast cells ; Rat hindquarter perfusion
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 1. The basic peptide substance P causes histamine release from peritoneal mast cells of the rat in vitro whereas the closely related neutral peptides eledoisin and physalaemin do not. 2. Infusion of substance P (7.4 nmol min−1), but not of eledoisin (8.4 nmol min−1) or physalaemin (7.9 nmol min−1), into the rat hindquater preparation caused a more than 4-fold increase of the histamine content in the venous outflow. The outflow of 5-HT remained unchanged under infusion of all three peptides. 3. No histamine depletion in the skin of the rat hind paw was observed following antidromic stimulation of the saphenous nerve or cutaneous application of mustard oil. Infusion of substance P (7.4 nmol min−1) caused a 47% depletion of histamine in the paw skin although only a small proportion of the infused substance P seemed to enter the tissue from the blood vessels. 4. The results further substantiate the view that substance P upon release from peripheral nerve endings induces release of histamine from cutaneous mast cells, a mechanism which contributes to neurogenic vasodilatation and plasma extravasation.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 336 (1987), S. 316-320 
    ISSN: 1432-1912
    Keywords: Acetylcholine ; [d-Met2, Pro5]-enkephalin-amide ; Prostaglandin E2 ; Capsaicin ; Sensory nerves
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effect of a potent opioid agonist, [d-Met2, Pro5]-enkephalinamide was investigated on two responses involving capsaicin-sensitive afferent neurones, namely, atropine-resistant contractions of the guinea-pig bronchus evoked by electrical field stimulation and the nociceptor stimulation to intraarterial injections of acetylcholine or capsaicin into the vascularly isolated rabbit ear. The hypotheses to be tested were whether (a) opioid receptor activation may inhibit mediator release from primary afferent neurones and (b) the opioid could exert an analgesic effect at a peripheral site of action. Non-cholinergic contractions of the guinea-pig isolated main bronchi due to electrical stimulation were concentration-dependently inhibited by [d-Met2, Pro5]-enkephalinamide (10 nM–1 μM). This effect was abolished by naloxone (1 μM). Naloxone alone induced no change in the stimulation-evoked contractions of the bronchus, indicating that no endogenous opioid control was present. Substance P and neurokinin A induced bronchial contractions that were not influenced by [d-Met2, Pro5]-enkephalinamide. This indicates that [d-Met2, Pro5]-enkephalinamide inhibits electrically-evoked bronchial contractions by reduced mediator release from capsaicin-sensitive sensory nerve endings, since these contractions are most probably brought about by tachykinins, released from afferent neurones. Capsaicin-induced bronchial contractions were in contrast to electrical stimulation not influenced by [d-Met2, Pro5]-enkephalinamide which suggests a different site of action. The activation of sensory neurones in the rabbit ear by i. a. injection of acetylcholine and capsaicin was not reduced under infusion of [d-Met2, Pro5]-enkephalinamide (1 and 10 μM) or lofentanil (1 and 10 μM). The enhancement of the effect of acetylcholine by infusion of prostaglandin E2 (0.15 μM) also remained unchanged under infusion of 10 μM [d-Met2, Pro5]-enkephalinamide. A peripheral analgesic action of the two opioid agonists studied is therefore not indicated.
    Type of Medium: Electronic Resource
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