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Ileal Longitudinal Muscle (ileal + longitudinal_muscle)

Distribution by Scientific Domains
Medical Sciences100%

Kinds of Ileal Longitudinal Muscle

  • guinea-pig ileal longitudinal muscle
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    Selected Abstracts

    Inhibition of oxotremorine-induced desensitization of guinea-pig ileal longitudinal muscle in Ca2+ -free conditions

    JOURNAL OF PHARMACY AND PHARMACOLOGY: AN INTERNATI ONAL JOURNAL OF PHARMACEUTICAL SCIENCE, Issue 2 2001
    Shuhei Horio
    The aim of this study was to investigate the differences between oxotremorine-induced and acetylcholine (ACh)-induced desensitization, particularly under Ca2+ -free conditions, in guinea-pig ileal longitudinal muscle, and to elucidate the different mechanisms of desensitization that might exist between these two muscarinic agonists. Pretreatment of the tissue with 10,7 , 10,5 M oxotremorine (desensitizing treatment) in normal Tyrode solution caused desensitization of the responses to ACh, as did the desensitizing treatment with ACh. However, Ca2+ -free conditions significantly reduced oxotremorine-induced desensitization, contrary to the previous findings that Ca2+ -free conditions enhanced ACh-induced desensitization. The desensitizing treatment with oxotremorine caused suppression of the responses to high K+ (tonic phase), as did the ACh treatment. Ca2+ -free conditions removed this suppression, whereas this condition enhanced ACh-induced suppression of the K+ response. A protein kinase C inhibitor, 1-(5-isoquinolinesulfonyl)-2-methylpiperazine (10,4 M) had no effect on oxotremorine-induced desensitization of the ACh response. The results suggest that a voltage-gated Ca2+ channel was involved in oxotremorine-induced desensitization, as in ACh-induced desensitization, but that the process of inactivation of Ca2+ channels was different between oxotremorine and ACh, and that oxotremorine-induced desensitization was due not only to Ca2+ channel, but also to other unknown factors. Protein kinase C did not participate in oxotremorine-induced desensitization. [source]

    Cholinergic responses of ileal longitudinal muscle under short-lasting exposure to cupric ions

    AUTONOMIC & AUTACOID PHARMACOLOGY, Issue 1 2008
    Ch. Nachev
    Summary 1 The effect of short-term exposure to cupric ions (Cu2+) on electric field-stimulated (EFS) or agonist-induced contractions of guinea-pig isolated ileum was studied. 2 EFS elicited tetrodotoxin- and atropine-sensitive contractions that were concentration dependently inhibited by Cu2+ (IC50 = 14.7 ± 4.2 ,m). Maximal inhibition (90.4 ± 3.1% of baseline contractions) was attained with 30 ,m Cu2+. 3 Carbachol induced concentration-dependent contractions (EC50 = 0.021 ± 0.004 ,m) that were inhibited by 0.3 ,m atropine to a non-competitive manner (decreased maximal response, EC50 value = 0.26 ± 0.04 ,m, Ke = 0.026 ,m). Cu2+ (15 ,m) potentiated contractions induced by carbachol, such that the maximum response was increased by 30.3 ± 10.4%. 4 Histamine induced concentration-dependent contractions of the longitudinal muscle (EC50 = 0.11 ± 0.03 ,m). Dyphenhydramine (0.1 ,m) decreased the maximum response to histamine and shifted the curve to the right (EC50 value = 4.71 ± 0.35 ,m, Ke = 0.0024 ,m). Cu2+ (15 ,m) caused a rightward shift of the histamine concentration,response curve (EC50 = 0.61 ± 0.1 ,m) without changing the maximum response. Serotonin induced concentration-dependent contractions at concentrations higher than 10 nM (EC50 value of 0.34 ± 0.12 ,m) were not significantly affected by 15 ,m Cu2+. 5 Our results suggest that in ileal longitudinal muscle, Cu2+ inhibits cholinergic neurotransmission but also facilitates postsynaptic muscarinic receptor responses. [source]

    Long-lasting contractile action and the inhibitory action of cupric ions on ileal longitudinal muscle

    AUTONOMIC & AUTACOID PHARMACOLOGY, Issue 4 2004
    K. Miyazaki
    Summary 1 Cupric ions (Cu2+), at concentrations above 0.03 mm, induced a progressive increase in the tonic contraction of guinea-pig ileal longitudinal muscle. Maximal contraction of 0.1 mm Cu2+ attained a level above that of the 60-mm K+ -induced tonic response, within 20 min of application. The tension induced by Cu2+ persisted for more than several hours. Tetrodotoxin (3 × 10,6 m) had no effect on the contraction induced by 0.1 mm Cu2+. 2 After incubation in a Ca2+ -free medium, the ileal response to 0.1 mm Cu2+ was lost. Nifedipine, a L-type Ca2+ channel blocker, dose-dependently inhibited contractions induced by Cu2+. 3 As the duration of the first application of 0.1 mm Cu2+ increased above 30 min, after washing with normal medium, the contractile response to a second application of 0.1 mm Cu2+ decreased gradually. After 150 min of the first application of 0.1 mm Cu2+, a second application of Cu2+ could not evoke any contraction. 4 After the application of 0.1 mm Cu2+ for 150 min, when muscles were washed with a medium containing 1 mm EDTA, the response to 0.1 mm Cu2+ returned to a greater extent in the normal Ca2+ medium. 5 In conclusion, Cu2+ (0.1 mm) induced a maximal ileal tension above that of the K-induced tonic response within 20 min. The ileal contraction to Cu2+ persisted for more than several hours and depended on extracellular Ca2+ concentrations. It is possible that a part of Cu2+, bound to a EDTA-inaccessible site, also has a tension inhibitory effect. [source]

    Receptor signaling mechanisms underlying muscarinic agonist-evoked contraction in guinea-pig ileal longitudinal smooth muscle

    BRITISH JOURNAL OF PHARMACOLOGY, Issue 2 2003
    T Unno
    In guinea-pig ileal longitudinal muscle, muscarinic partial agonists, 4-(N -[3-chlorophenyl]-carbomoyloxy)-2-butynyl-trimethylammonium (McN-A343) and pilocarpine, each produced parallel increases in tension and cytosolic Ca2+ concentration ([Ca2+]c) with a higher EC50 than that of the full agonist carbachol. The maximum response of [Ca2+]c or tension was not much different among the three agonists. The Ca2+ channel blocker nicardipine markedly inhibited the effects of all three agonists The contractile response to any agonist was antagonized in a competitive manner by M2 receptor selective antagonists (N,N,- bis[6-[[(2-methoyphenyl)methyl]amino]hexyl]-1,8-octanediamine tetrahydrochloride and 11-[[2-[(diethlamino)methyl]-1-piperidinyl]acetyl]-5,11-dihydro-6H-pyrido[2,3-b][1,4] benzodiazepine-6-one), and the apparent order of M2 antagonist sensitivity was McN-A343>pilocarpine>carbachol. M3 receptor selective antagonists, 1,1-dimethyl-4-diphenylacetoxypiperidinium iodide and darifenacin, both severely depressed the maximum response for McN-A343, while darifenacin had a similar action in the case of pilocarpine. Both M3 antagonists behaved in a competitive manner in the case of the carbachol response. McN-A343 failed to release Ca2+ from the intracellular stores, and the Ca2+ -releasing action of pilocarpine was very weak compared with that of carbachol. All three agonists were capable of increasing Ca2+ sensitivity of the contractile proteins. McN-A343 rarely produced membrane depolarization, but always accelerated electrical spike discharge. Pilocarpine effect was more often accompanied by membrane depolarization, as was usually seen using carbachol. The results suggest that muscarinic agonist-evoked contractions result primarily from the integration of Ca2+ entry associated with the increased spike discharge and myofilaments Ca2+ sensitization, and that Ca2+ store release may contribute to the contraction indirectly via potentiation of the electrical membrane responses. They may also support the idea that an interaction of M2 and M3 receptors plays a crucial role in mediating the contraction response. British Journal of Pharmacology (2003) 139, 337,350. doi:10.1038/sj.bjp.0705267 [source]