Arginine vasopressin, via activation of post-junctional V1 receptors, induces contractileeffects in mouse distal colon

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Abstract

The aim of this study was to analyze whether arginine vasopressin (AVP) may be considered a modulator ofintestinal motility. In this view, we evaluated, in vitro, the effects induced by exogenous administration of AVPon the contractility of mouse distal colon, the subtype(s) of receptor(s) activated and the action mechanism.Isometric recordings were performed on longitudinal and circular muscle strips of mouse distal colon. AVP(0.001 nM–100 nM) caused concentration-dependent contractile effects only on the longitudinal muscle,antagonized by the V1 receptor antagonist, V-1880. AVP-induced effect was not modified by tetrodotoxin,atropine and indomethacin. Contractile response to AVP was reduced in Ca2+-free solution or in the presenceof nifedipine, and it was abolished by depletion of calcium intracellular stores after repetitive addition of carbacholin calcium-freemediumwith addition of cyclopiazonic acid.U-73122, an inhibitor of the phospholipase C, effectivelyantagonized AVP effects, whilst it was not affected by an adenylyl cyclase inhibitor. Oxytocin induced an excitatoryeffect in the longitudinalmuscle of distal colon at very high concentrations, effect antagonized by V-1880. The resultsof this study shown that AVP, via activation of V1 receptors, is able to modulate positively contractile activity oflongitudinal muscle of mouse distal colon, independently by enteric nerve activation and prostaglandin synthesis.Contractile response is achieved by increase in cytoplasmatic Ca2+ concentration via extracellular Ca2+ influx from L-type Ca2+ channels and via Ca2+ release from intracellular stores through phospholipase C pathway.No modulation has been observed on the contractility of the circular muscle.
Original languageEnglish
Pages (from-to)29-34
Number of pages6
JournalRegulatory Peptides
Volume187
Publication statusPublished - 2013

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Vasopressin Receptors
Arginine Vasopressin
Colon
Chemical activation
Muscle
Muscles
Type C Phospholipases
Calcium
Tetrodotoxin
Oxytocin
Nifedipine
Atropine
Adenylyl Cyclases
Indomethacin
Modulators
Prostaglandins
Modulation

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Physiology
  • Endocrinology
  • Clinical Biochemistry
  • Cellular and Molecular Neuroscience

Cite this

@article{e82c4ef2eb1f432b8d66d36f4ca631f5,
title = "Arginine vasopressin, via activation of post-junctional V1 receptors, induces contractileeffects in mouse distal colon",
abstract = "The aim of this study was to analyze whether arginine vasopressin (AVP) may be considered a modulator ofintestinal motility. In this view, we evaluated, in vitro, the effects induced by exogenous administration of AVPon the contractility of mouse distal colon, the subtype(s) of receptor(s) activated and the action mechanism.Isometric recordings were performed on longitudinal and circular muscle strips of mouse distal colon. AVP(0.001 nM–100 nM) caused concentration-dependent contractile effects only on the longitudinal muscle,antagonized by the V1 receptor antagonist, V-1880. AVP-induced effect was not modified by tetrodotoxin,atropine and indomethacin. Contractile response to AVP was reduced in Ca2+-free solution or in the presenceof nifedipine, and it was abolished by depletion of calcium intracellular stores after repetitive addition of carbacholin calcium-freemediumwith addition of cyclopiazonic acid.U-73122, an inhibitor of the phospholipase C, effectivelyantagonized AVP effects, whilst it was not affected by an adenylyl cyclase inhibitor. Oxytocin induced an excitatoryeffect in the longitudinalmuscle of distal colon at very high concentrations, effect antagonized by V-1880. The resultsof this study shown that AVP, via activation of V1 receptors, is able to modulate positively contractile activity oflongitudinal muscle of mouse distal colon, independently by enteric nerve activation and prostaglandin synthesis.Contractile response is achieved by increase in cytoplasmatic Ca2+ concentration via extracellular Ca2+ influx from L-type Ca2+ channels and via Ca2+ release from intracellular stores through phospholipase C pathway.No modulation has been observed on the contractility of the circular muscle.",
author = "Michelangelo Auteri and Serio, {Rosa Maria} and Flavia Mule' and Mariangela Mastropaolo and Zizzo, {Maria Grazia}",
year = "2013",
language = "English",
volume = "187",
pages = "29--34",
journal = "Regulatory Peptides",
issn = "0167-0115",
publisher = "Elsevier",

}

TY - JOUR

T1 - Arginine vasopressin, via activation of post-junctional V1 receptors, induces contractileeffects in mouse distal colon

AU - Auteri, Michelangelo

AU - Serio, Rosa Maria

AU - Mule', Flavia

AU - Mastropaolo, Mariangela

AU - Zizzo, Maria Grazia

PY - 2013

Y1 - 2013

N2 - The aim of this study was to analyze whether arginine vasopressin (AVP) may be considered a modulator ofintestinal motility. In this view, we evaluated, in vitro, the effects induced by exogenous administration of AVPon the contractility of mouse distal colon, the subtype(s) of receptor(s) activated and the action mechanism.Isometric recordings were performed on longitudinal and circular muscle strips of mouse distal colon. AVP(0.001 nM–100 nM) caused concentration-dependent contractile effects only on the longitudinal muscle,antagonized by the V1 receptor antagonist, V-1880. AVP-induced effect was not modified by tetrodotoxin,atropine and indomethacin. Contractile response to AVP was reduced in Ca2+-free solution or in the presenceof nifedipine, and it was abolished by depletion of calcium intracellular stores after repetitive addition of carbacholin calcium-freemediumwith addition of cyclopiazonic acid.U-73122, an inhibitor of the phospholipase C, effectivelyantagonized AVP effects, whilst it was not affected by an adenylyl cyclase inhibitor. Oxytocin induced an excitatoryeffect in the longitudinalmuscle of distal colon at very high concentrations, effect antagonized by V-1880. The resultsof this study shown that AVP, via activation of V1 receptors, is able to modulate positively contractile activity oflongitudinal muscle of mouse distal colon, independently by enteric nerve activation and prostaglandin synthesis.Contractile response is achieved by increase in cytoplasmatic Ca2+ concentration via extracellular Ca2+ influx from L-type Ca2+ channels and via Ca2+ release from intracellular stores through phospholipase C pathway.No modulation has been observed on the contractility of the circular muscle.

AB - The aim of this study was to analyze whether arginine vasopressin (AVP) may be considered a modulator ofintestinal motility. In this view, we evaluated, in vitro, the effects induced by exogenous administration of AVPon the contractility of mouse distal colon, the subtype(s) of receptor(s) activated and the action mechanism.Isometric recordings were performed on longitudinal and circular muscle strips of mouse distal colon. AVP(0.001 nM–100 nM) caused concentration-dependent contractile effects only on the longitudinal muscle,antagonized by the V1 receptor antagonist, V-1880. AVP-induced effect was not modified by tetrodotoxin,atropine and indomethacin. Contractile response to AVP was reduced in Ca2+-free solution or in the presenceof nifedipine, and it was abolished by depletion of calcium intracellular stores after repetitive addition of carbacholin calcium-freemediumwith addition of cyclopiazonic acid.U-73122, an inhibitor of the phospholipase C, effectivelyantagonized AVP effects, whilst it was not affected by an adenylyl cyclase inhibitor. Oxytocin induced an excitatoryeffect in the longitudinalmuscle of distal colon at very high concentrations, effect antagonized by V-1880. The resultsof this study shown that AVP, via activation of V1 receptors, is able to modulate positively contractile activity oflongitudinal muscle of mouse distal colon, independently by enteric nerve activation and prostaglandin synthesis.Contractile response is achieved by increase in cytoplasmatic Ca2+ concentration via extracellular Ca2+ influx from L-type Ca2+ channels and via Ca2+ release from intracellular stores through phospholipase C pathway.No modulation has been observed on the contractility of the circular muscle.

UR - http://hdl.handle.net/10447/86712

M3 - Article

VL - 187

SP - 29

EP - 34

JO - Regulatory Peptides

JF - Regulatory Peptides

SN - 0167-0115

ER -