Library

X
feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    Electronic Resource
    Electronic Resource
    Effects of substance P, cholecystokinin octapeptide, bombesin, and neurotensin on the peristaltic reflex of the guinea-pig ileum in the absence and in the presence of atropine (1982)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 321 (1982), S. 321-328 
    Details
    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
    URL: http://dx.doi.org/10.1007/BF00498521
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 2
    Electronic Resource
    Electronic Resource
    The site of action of capsaicin on the guinea-pig isolated ileum (1978)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 305 (1978), S. 75-81 
    Details
    ISSN: 1432-1912
    Keywords: Capsaicin ; Cholinergic mechanism ; Periarterial mesenteric nerves ; Sensory fibres ; Ileum innervation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The site and mode of action of capsaicin were analysed on the guinea-pig isolated ileum. 1. Capsaicin produced longitudinal contraction (EC50 4.2×10−8 g/ml) followed by a specific, rapid and irreversible tachyphylaxis (IC50 2.8×10−7 g/ml). 2. Capsaicin was ineffective in the presence of tetrodotoxin (2×10−7 g/ml) or on ilea kept for 24–48 h at 4°C, without an oxygen supply. 3. On ileal segments, the perivascular mesenteric nerves of which were transsected 5–8 days before the experiment, practically no response to capsaicin was obtained. Chronic abdominal bilateral vagotomy was without any effect. 4. Hyoscine (1×10−8–1×10−6 g/ml) or morphine (2×10−6 g/ml) strongly inhibited contractions produced by capsaicin. Neither mecamylamine (1×10−5 g/ml), nor nicotine (5×10−5 g/ml) and dimethylphenylpiperazinium (5×10−6 g/ml) caused any change, while an increased response to capsaicin was obtained in the presence of hexamethonium (1×10−4 g/ml). 5. Unaltered contractions were produced by capsaicin on ileal segments made tachyphylactic to 5-HT, bradykinin or substance P. Histamine antagonists at H1 and H2 receptors (chloropyramine, burimamide), the prostaglandin synthesis inhibitor indomethacin, pretreatment with the adrenergic neuron blocking agent guanethidine, as well as in vivo reserpine pretreatment were also ineffective in this respect. 6. It is concluded that in the guinea-pig ileum capsaicin causes predominantly cholinergic contraction by stimulating terminals of extrinsic, non-parasympathetic nerves.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00497008
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    New type of nerve-mediated cholinergic contractions of the guinea-pig small intestine and its selective blockade by capsaicin (1978)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 305 (1978), S. 83-90 
    Details
    ISSN: 1432-1912
    Keywords: Capsaicin ; Cholinergic mechanism ; Periarterial mesenteric nerves ; Sensory fibres ; Ileum innervation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 1. Electrical stimulation (2–50Hz) of mesenteric nerves of the guinea-pig isolated ileum resulted in contraction of preparations pretreated with adrenergic neuron blocking agents (guanethidine, bretylium), or on preparations obtained from animals pretreated with reserpine. Stimulation at low frequencies (2–10 Hz) also caused contraction in untreated preparations. 2. The response was abolished by hyoscine (1 ×10−7–1×10−6 g/ml) or morphine (2×10−7 g/ml). However, previous bilateral vagotomy, hexamethonium (1×10−4 g/ml), mecamylamine (1×10−5 g/ml), or desensitization of the gut to 5-HT caused practically no inhibition. 3. Capsaicin inhibited or abolished (IC50 1.5 ×10−8 g/ml) the contraction elicited by stimulation of mesenteric nerves in an irreversible manner. The drug did not inhibit the contraction to field stimulation of the postganglionic cholinergic fibres. 4. Neither the contraction of the duodenum to stimulation of the preganglionic vagal fibres, nor the adrenergic inhibition elicited by periarterial nerve stimulation were influenced by capsaicin. 5. It is concluded that the cholinergic response described above is neither parasympathetic in origin nor can it explained on the basis of a cholinergic mechanism in adrenergic neurotransmission (Burn's theory). A hypothesis is put forward that nerve fibres characterized by their specific sensitivity to capsaicin, presumably originating from sensory neurons excite cholinergic neurons of the myenteric plexus.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00497009
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...