Apamin‐sensitive and ‐insensitive components of inhibitory junction potentials in rat caecum: role of nitric oxide

Serio, Rosa; Mulè, Flavia; Postorino, A.; Vetri, T.; Bonvissuto, F.

doi:10.1111/j.1474-8673.1996.tb00421.x

Cited by 17 publications

(10 citation statements)

References 30 publications

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“…EFS-induced fast inhibitory junction potentials (i.j.ps) were suggested to be mediated by ATP and to be apamin-sensitive in the circular muscle of the human jejunum (11), the guinea pig ileum (12), the rat colon (13), the guinea pig colon (14), and the mouse distal colon (15). Although these results suggest a role of ATP in NANC relaxation, several reports present contradictory results: no role for ATP was suggested in the rat ileum (16), proximal colon (17), and caecum (18) and the guinea pig gastric fundus (19). This discrepancy may be due to the regional, species, and strain differences in the mediator of NANC relaxation (20,21).…”

Section: Introductionmentioning

confidence: 55%

Participation of ATP in Nonadrenergic, Noncholinergic Relaxation of Longitudinal Muscle of Wistar Rat Jejunum

et al. 2005

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Abstract. A role of ATP in nonadrenergic, noncholinergic (NANC) relaxations was examined in the Wistar rat jejunum. Electrical field stimulation (EFS) induced NANC relaxation of longitudinal muscle of the jejunal segments in a frequency-dependent manner. A purinoceptor antagonist, adenosine 3'-phosphate 5'-phosphosulfate (A3P5PS, 100 mM) inhibited the relaxation: relaxations induced by EFS at lower or higher frequencies were either completely or partially inhibited, respectively. After the jejunal segments had been desensitized to ATP, the relaxations were decreased to the same extent as those inhibited by A3P5PS. An inhibitor of small conductance Ca 2+-activated K + channels (SK channels), apamin (100 nM), completely inhibited EFS-induced relaxations. Treatment of the segments with an inhibitor of sarcoplasmic reticulum Ca 2+ -ATPase, thapsigargin (1 mM), significantly inhibited the relaxations. The exogenous ATPinduced relaxation of longitudinal muscle occurred with a concomitant decrease in intracellular Ca 2+ levels. Apamin and thapsigargin abolished these ATP-induced responses. A3P5PS significantly inhibited the inhibitory junction potentials which were induced in the longitudinal muscle cells. In addition, apamin significantly inhibited the hyperpolarization that was induced by exogenous ATP in the cells. These findings in the Wistar rat jejunum suggest that ATP participates in the NANC relaxation via activation of SK channels induced by Ca 2+ ions that are released from the thapsigargin-sensitive store site.

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Section: Introductionmentioning

confidence: 55%

Participation of ATP in Nonadrenergic, Noncholinergic Relaxation of Longitudinal Muscle of Wistar Rat Jejunum

et al. 2005

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“…Studies, in which neurogenic transient hyperpolarizations – known as inhibitory junction potentials (IJP) – were studied, show a fast and a slow component of hyperpolarization in response to NANC nerve stimulation. Some authors proposed ATP as the mediator of the fast APA‐sensitive IJP component, whereas NO is proposed as the NANC neurotransmitter responsible for the slow APA‐insensitive component in circular muscle strips of human colon, 48 guinea pig colon, 49 Sprague–Dawley rat colon 40 and Wistar rat caecum 50 . Others have claimed NO to be responsible for the APA‐sensitive component of IJP in Wistar rat colon circular muscle, 20,51 canine intestine circular muscle 21 or even to be involved in both the fast and the slow IJP component as was described for hamster ileum circular muscle 28 …”

Section: Responses To Efsmentioning

confidence: 99%

Nitrergic–purinergic interactions in rat distal colon motility

Crombruggen

Lefebvre

2004

Neurogastroenterology Motil

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Responses of rat distal colon circular muscle strips to exogenous nitric oxide (NO) and adenosine 5'-triphosphate (ATP) and to electrical field stimulation (EFS) were assessed in the absence/presence of various agents that interfere with nitrergic-purinergic pathways. Exogenous NO (10-6 to 10-4 mol L-1) elicited concentration-dependent, tetrodotoxin (TTX)-insensitive relaxations. The soluble guanylyl-cyclase (sGC) inhibitor 1H[1,2,4,]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ) reduced duration and amplitude; the small conductance Ca2+-sensitive K+ (SK)-channel blocker apamin (APA) only shortened the relaxations. ODQ + APA showed a marked inhibitory effect on duration and amplitude. TTX, APA, the NO-synthase inhibitor N(omega)-nitro-l-arginine methyl ester (l-NAME) and the purinergic receptor P2Y antagonist Reactive Blue 2 (RB2) shortened the relaxations by exogenous ATP (10-3 mol L-1) but did not influence the amplitude. ODQ had no effect. TTX + l-NAME did not yield a more pronounced inhibitory effect than TTX alone. The effect of ATP-gamma-S was similar to that of ATP. Electrical field stimulation (EFS) (40 V, 0.05 ms, 0.5-4 Hz for 30 s) yielded TTX-sensitive relaxations that were not altered by l-NAME, ODQ or RB2. APA shortened the relaxations. l-NAME + APA nearly abolished these relaxations. ODQ + APA and RB2 +l-NAME reduced the duration. These results suggest that distinct sets of small conductance SK-channels are involved in the amplitude and the duration of the relaxations and that NO increases their sensitivity to NO and ATP via guanosine 3',5'-cyclic monophosphate (cGMP). ATP elicits relaxations via P2Y receptors with subsequent activation of SK-channels and induces neuronal release of NO. Both nitrergic and purinergic pathways must be blocked to inhibit EFS-induced relaxations.

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“…In the presence of apamin, EJPs and depolarisations were evoked by ATP, which were not blocked by indomethacin (Shuba and Vladimirova 1980). The inhibitory responses of the caecum of the rat (which has no taenia coli) have been described (Mehta and Kulkarni 1983) and Reactive blue 2 was shown to reduce the IJPs and hyperpolarisations to a,b-meATP in this preparation (Manzini et al 1986), although this was contested in a later paper (Serio et al 1996). Inhibitory transmission to the longitudinal muscle of the mouse caecum was claimed to be mediated largely by NO (Young et al 1996).…”

Section: Caecum and Taenia Colimentioning

confidence: 88%