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  • Articles: DFG German National Licenses  (2)
  • Cholecystokinin octapeptide  (1)
  • Key words Taenia caeci (guinea-pig)  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 358 (1998), S. 496-499 
    ISSN: 1432-1912
    Keywords: Key words Taenia caeci (guinea-pig) ; Nitric oxide ; NG-nitro-l-arginine ; P2 purinoceptors ; PPADS
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effect of the nitric oxide synthase inhibitor N G-nitro-l-arginine (l-NOARG; 100 µM) and the P2 purinoceptor antagonist pyridoxalphosphate-6-azophenyl-2’,4’-disulfonic acid (PPADS; 50 µM) was investigated on the non-adrenergic, non-cholinergic (NANC) relaxant response of the guinea-pig isolated taenia caeci to electrical field stimulation at 1 or 10 Hz, under isotonic recording conditions. Either drug alone caused an about 50% inhibition, while combining the two drugs nearly abolished the response at both frequencies. The inhibitory effect of l-NOARG (100 µM) was partly reversed by l-arginine (30 mM). PPADS, but not l-NOARG, inhibited the relaxant effect of exogenous ATP, but not that of the nitric oxide donor sodium nitroprusside. It is concluded that both nitric oxide and ATP are involved in the mediation of NANC relaxation in the taenia caeci, in an apparently additive manner.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-1912
    Keywords: Peristaltic reflex ; Atropine-resistant peristalsis ; Guinea-pig ileum ; Substance P ; Cholecystokinin octapeptide ; Bombesin ; Neurotensin ; Naloxone
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 1. Slow peristalsis (less than one peristaltic wave/min) was induced by continuous elevation of intraluminal pressure in vascularly perfused segments of the guinea-pig isolated ileum. The intraluminal pressure at the aboral side of the segment and the volume of fluid propelled by each peristaltic wave were recorded. 2. Intraarterial infusion of substance P (11.5–115 pmoles min−1), cholecystokinin octapeptide (CCK-8; 1.5–15 pmoles min−1), bombesin (1–10 pmoles min−1), and neurotensin (3.6–36 pmoles min−1) dose-dependently stimulated peristalsis, the degree of stimulation being largest with CCK-8. Histamine, a drug contracting the smooth muscle directly, did not stimulate peristalsis. 3. Atropine (1 μM in the bath and perfusion solution) caused a transient inhibition or blockade of the peristaltic reflex, followed by a partial recovery of peristalsis (“atropine-resistant peristalsis”). Atropine-resistant peristalsis was greatly stimulated by CCK-8 (6–15 pmoles min−1), only slightly stimulated by bombesin (4 pmoles min−1), and first stimulated and then inhibited by neurotensin (36 pmoles min−1). 4. Substance P (11.5–1,000 pmoles min−1) inhibited or abolished atropine-resistant peristalsis, which was probably due to desensitization of intestinal smooth muscle and/or neurones against the peptide. [d-Pro2, d-Trp7,9] substance P, an analogue of substance P with antagonistic properties (40 nmoles min−1), also inhibited atropine-resistant peristalsis. 5. Naloxone (4.6 nmoles min−1) stimulated peristalsis both in the absence and in the presence of atropine; this indicates that endogenous opioids modulate peristaltic motility. 6. It is concluded that neuropeptides stimulate peristalsis by exciting intramural cholinergic and non-cholinergic neurones. The inhibitory actions of substance P desensitization and of the substance P antagonist in the presence of atropine indicate that substance P neurones play a role in the mechanism af the atropine-resistant peristalsis.
    Type of Medium: Electronic Resource
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