Activation of P2Y receptors by ATP and by its analogue, ADPbetaS, triggers two calcium signal pathways in the longitudinal muscle of mouse distal colon.

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Abstract

Our previous research showed that ATP and adenosine 5'-O-2-thiodiphosphate (ADPbetaS) induce contractile effects in the longitudinal muscle of mouse distal colon via activation of P2Y receptors which are not P2Y(1) or P2Y(12) subtypes. This study investigated the nature of the P2Y receptor subtype(s) and the mechanisms leading to the intracellular calcium concentration increase necessary to trigger muscular contraction. Motor responses of mouse colonic longitudinal muscle to P2Y receptor agonists were examined in vitro as changes in isometric tension. ATP or ADPbetaS induced muscular contraction, which was not affected by P2Y(11) or P2Y(13) selective antagonists. Calcium-free solution or the calcium channel blocker, nifedipine, failed to modify the contractile responses to ATP or ADPbetaS, which were virtually abolished by depletion of calcium intracellular stores after repetitive addition of carbachol in calcium-free medium with addition of cyclopiazonic acid. Neomycin or U-73122, phospholipase C inhibitors, or 2-aminoethoxy-diphenylborate (2-APB), membrane-permeant IP(3) receptor inhibitor reduced the response to ATP, whilst ryanodine or ruthenium red, inhibiting calcium release from ryanodine-sensitive stores, abolished the response to ADPbetaS. Responses to maximally effective concentrations of ATP and ADPbetaS were not fully additive. Desensitisation with ADPbetaS antagonized the contractile effects of ATP, as desensitisation with ATP antagonized the response to ADPbetaS. In the longitudinal muscle of mouse distal colon, ATP and ADPbetaS induce muscular contraction via a P2Y receptor, coupled to differential signal pathways leading to intracellular calcium increase.
Lingua originaleEnglish
pagine (da-a)84-89
Numero di pagine6
RivistaEuropean Journal of Pharmacology
Volume595(1-3)
Stato di pubblicazionePublished - 2008

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Purinergic P2 Receptors
Signal Transduction
Colon
Adenosine Triphosphate
Calcium
Muscles
Muscle Contraction
Ryanodine
adenosine 5'-O-(2-thiodiphosphate)
Ruthenium Red
Neomycin
Calcium Channel Blockers
Carbachol
Type C Phospholipases
Nifedipine

All Science Journal Classification (ASJC) codes

  • Pharmacology

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title = "Activation of P2Y receptors by ATP and by its analogue, ADPbetaS, triggers two calcium signal pathways in the longitudinal muscle of mouse distal colon.",
abstract = "Our previous research showed that ATP and adenosine 5'-O-2-thiodiphosphate (ADPbetaS) induce contractile effects in the longitudinal muscle of mouse distal colon via activation of P2Y receptors which are not P2Y(1) or P2Y(12) subtypes. This study investigated the nature of the P2Y receptor subtype(s) and the mechanisms leading to the intracellular calcium concentration increase necessary to trigger muscular contraction. Motor responses of mouse colonic longitudinal muscle to P2Y receptor agonists were examined in vitro as changes in isometric tension. ATP or ADPbetaS induced muscular contraction, which was not affected by P2Y(11) or P2Y(13) selective antagonists. Calcium-free solution or the calcium channel blocker, nifedipine, failed to modify the contractile responses to ATP or ADPbetaS, which were virtually abolished by depletion of calcium intracellular stores after repetitive addition of carbachol in calcium-free medium with addition of cyclopiazonic acid. Neomycin or U-73122, phospholipase C inhibitors, or 2-aminoethoxy-diphenylborate (2-APB), membrane-permeant IP(3) receptor inhibitor reduced the response to ATP, whilst ryanodine or ruthenium red, inhibiting calcium release from ryanodine-sensitive stores, abolished the response to ADPbetaS. Responses to maximally effective concentrations of ATP and ADPbetaS were not fully additive. Desensitisation with ADPbetaS antagonized the contractile effects of ATP, as desensitisation with ATP antagonized the response to ADPbetaS. In the longitudinal muscle of mouse distal colon, ATP and ADPbetaS induce muscular contraction via a P2Y receptor, coupled to differential signal pathways leading to intracellular calcium increase.",
keywords = "ATP, Intracellular calcium store, Muscular contraction, P2Y purinoreceptor",
author = "Zizzo, {Maria Grazia} and Serio, {Rosa Maria} and Flavia Mule'",
year = "2008",
language = "English",
volume = "595(1-3)",
pages = "84--89",
journal = "European Journal of Pharmacology",
issn = "0014-2999",
publisher = "Elsevier",

}

TY - JOUR

T1 - Activation of P2Y receptors by ATP and by its analogue, ADPbetaS, triggers two calcium signal pathways in the longitudinal muscle of mouse distal colon.

AU - Zizzo, Maria Grazia

AU - Serio, Rosa Maria

AU - Mule', Flavia

PY - 2008

Y1 - 2008

N2 - Our previous research showed that ATP and adenosine 5'-O-2-thiodiphosphate (ADPbetaS) induce contractile effects in the longitudinal muscle of mouse distal colon via activation of P2Y receptors which are not P2Y(1) or P2Y(12) subtypes. This study investigated the nature of the P2Y receptor subtype(s) and the mechanisms leading to the intracellular calcium concentration increase necessary to trigger muscular contraction. Motor responses of mouse colonic longitudinal muscle to P2Y receptor agonists were examined in vitro as changes in isometric tension. ATP or ADPbetaS induced muscular contraction, which was not affected by P2Y(11) or P2Y(13) selective antagonists. Calcium-free solution or the calcium channel blocker, nifedipine, failed to modify the contractile responses to ATP or ADPbetaS, which were virtually abolished by depletion of calcium intracellular stores after repetitive addition of carbachol in calcium-free medium with addition of cyclopiazonic acid. Neomycin or U-73122, phospholipase C inhibitors, or 2-aminoethoxy-diphenylborate (2-APB), membrane-permeant IP(3) receptor inhibitor reduced the response to ATP, whilst ryanodine or ruthenium red, inhibiting calcium release from ryanodine-sensitive stores, abolished the response to ADPbetaS. Responses to maximally effective concentrations of ATP and ADPbetaS were not fully additive. Desensitisation with ADPbetaS antagonized the contractile effects of ATP, as desensitisation with ATP antagonized the response to ADPbetaS. In the longitudinal muscle of mouse distal colon, ATP and ADPbetaS induce muscular contraction via a P2Y receptor, coupled to differential signal pathways leading to intracellular calcium increase.

AB - Our previous research showed that ATP and adenosine 5'-O-2-thiodiphosphate (ADPbetaS) induce contractile effects in the longitudinal muscle of mouse distal colon via activation of P2Y receptors which are not P2Y(1) or P2Y(12) subtypes. This study investigated the nature of the P2Y receptor subtype(s) and the mechanisms leading to the intracellular calcium concentration increase necessary to trigger muscular contraction. Motor responses of mouse colonic longitudinal muscle to P2Y receptor agonists were examined in vitro as changes in isometric tension. ATP or ADPbetaS induced muscular contraction, which was not affected by P2Y(11) or P2Y(13) selective antagonists. Calcium-free solution or the calcium channel blocker, nifedipine, failed to modify the contractile responses to ATP or ADPbetaS, which were virtually abolished by depletion of calcium intracellular stores after repetitive addition of carbachol in calcium-free medium with addition of cyclopiazonic acid. Neomycin or U-73122, phospholipase C inhibitors, or 2-aminoethoxy-diphenylborate (2-APB), membrane-permeant IP(3) receptor inhibitor reduced the response to ATP, whilst ryanodine or ruthenium red, inhibiting calcium release from ryanodine-sensitive stores, abolished the response to ADPbetaS. Responses to maximally effective concentrations of ATP and ADPbetaS were not fully additive. Desensitisation with ADPbetaS antagonized the contractile effects of ATP, as desensitisation with ATP antagonized the response to ADPbetaS. In the longitudinal muscle of mouse distal colon, ATP and ADPbetaS induce muscular contraction via a P2Y receptor, coupled to differential signal pathways leading to intracellular calcium increase.

KW - ATP

KW - Intracellular calcium store

KW - Muscular contraction

KW - P2Y purinoreceptor

UR - http://hdl.handle.net/10447/36068

M3 - Article

VL - 595(1-3)

SP - 84

EP - 89

JO - European Journal of Pharmacology

JF - European Journal of Pharmacology

SN - 0014-2999

ER -