Effect of apamin on the electrical responses of smooth muscle to adenosine 5′-triphosphate and to non-adrenergic, non-cholinergic nerve stimulation

Shuba, M. F.; Vladimirova, I. A.

doi:10.1016/0306-4522(80)90154-2

Cited by 128 publications

(84 citation statements)

References 11 publications

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“…This i.j.p. was blocked by tetrodotoxin and apamin, and therefore this potential may be similar to that seen in smooth muscles of the mammalian gastrointestinal tract (Shuba & Vladimirova, 1980;Burnstock, 1981;Bauer & Kuriyama, 1982). The reversal potential of the i.j.p.…”

Section: Discussionmentioning

confidence: 74%

“…Smooth muscle cells ofthe guinea-pig stomach generate adrenergic i.j .p.s, cholinergic e.j.p.s and non-adrenergic, non-cholinergic i.j.p.s by stimulation of sympathetic or vagal nerves or by transmural nerve stimulation, among which the former potential is inhibited by drugs which block adrenergic transmission such as phentolamine or guanethidine, while the latter two are blocked by atropine and apamin, respectively (Kuriyama, Osa & Tasaki, 1970;Beani et al 1971;Bolton, 1979;Shuba & Vladimirova, 1980).…”

Section: Introductionmentioning

confidence: 99%

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Distribution and properties of excitatory and inhibitory junction potentials in circular muscle of the guinea‐pig stomach.

Komori¹,

Suzuki²

1986

The Journal of Physiology

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In the presence of guanethidine (10(‐6)‐5 X 10(‐6) M), transmural nerve stimulation evoked an excitatory junction potential (e.j.p.) in the fundus region and an inhibitory junction potential (i.j.p.) in the antrum region of the circular muscle of the guinea‐pig stomach. The e.j.p. was blocked by atropine (over 2 X 10(‐7) M) while the i.j.p. was blocked by apamin (10(‐7) M) but not by adrenergic or cholinergic receptor antagonists. Therefore the i.j.p. may be non‐adrenergic and non‐cholinergic in nature. In the presence of atropine, nerve stimulation evoked the non‐adrenergic, non‐cholinergic i.j.p. in both regions of the stomach. In the antrum region, single stimuli enhanced the subsequent slow wave by 1.1‐1.3 times, in comparison with that before the stimuli, and this effect was blocked by atropine (over 2 X 10(‐7) M). The reversal potential for the e.j.p. was about ‐18 mV, while that for the i.j.p. was ‐87 mV in the atropinized fundus and ‐89 mV in the antrum region. In the fundus region, a pair of nerve stimulations with short intervals (1‐4 s) reduced (depression) and with long intervals (5‐20 s) enhanced (facilitation) the second e.j.p. or the i.j.p. After inhibition of acetylcholine esterase (AChE) by physostigmine or neostigmine, nerve stimulation evoked an enhanced e.j.p., and then produced a sustained depolarization with a duration of 3‐5 s in the fundus region, while the amplitude of slow waves after nerve stimulation was further enhanced in the antrum region. These effects of anticholinesterases were blocked by atropine. Exogenously applied acetylcholine (ACh) depolarized the smooth muscle membrane; the threshold concentration of ACh was about 1000 times higher in the antrum region (10(‐6) M) than in the fundus region (10(‐9) M). It is concluded that in the guinea‐pig stomach, regional differences in junction potentials may be due to different sensitivities of ACh receptor, and that nerve stimulation evokes a cholinergic e.j.p. in a high‐sensitivity region (fundus) and a non‐adrenergic, non‐cholinergic i.j.p. in a low‐sensitivity region (antrum).

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Section: Discussionmentioning

confidence: 74%

Section: Introductionmentioning

confidence: 99%

Distribution and properties of excitatory and inhibitory junction potentials in circular muscle of the guinea‐pig stomach.

Komori¹,

Suzuki²

1986

The Journal of Physiology

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“…Others have shown that an extract from bee venom, apamin, inhibits ij.ps and neurally-mediated mechanical relaxations (Banks et al, 1979;Shuba & Vladimirova, 1980). Apamin has been shown to block small conductance, Ca2+-activated K channels in a variety of preparations (cf.…”

Section: Resultsmentioning

confidence: 99%

Role of nitric oxide in non‐adrenergic, non‐cholinergic inhibitory junction potentials in canine ileocolonic sphincter

Ward

McKeen

Sanders

1992

British J Pharmacology

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1 Electrical field stimulation causes neurally-mediated relaxation of the ileocolonic sphincter that is due to activation of non-adrenergic and non-cholinergic (NANC) nerves. Recent studies have suggested that nitric oxide (NO) is the neurotransmitter that mediates relaxation. 2 Using intracellular recording techniques, we have tested whether NANC inhibitory junction potentials (ij.ps) in the canine ileocolonic sphincter are also mediated by NO. 3 Electrical field stimulation elicited excitatory and inhibitory junction potentials: ej.ps were blocked by atropine (10-6 M) and tetrodotoxin (TTX; 10-6 M); ij.ps were also blocked by TTX and partially blocked by apamin (10-6 M). I.j.ps were unaffected by atropine, phentolamine and propranolol (all at 10-6 M). 4 The arginine analogues, L-N0-nitroarginine methyl ester (L-NAME) and N0-monomethyl-L-arginine (L-NMMA), decreased the amplitude of ij.ps and L-arginine, but not D-arginine, partially restored the '.J.ps.5 Ij.ps were also inhibited by oxyhaemoglobin (1%), but not by methaemoglobin. 6 Exogenous NO (1 -7M to 3 x 1 -5M) caused concentration-dependent hyperpolarizations that were similar in amplitude to the NANC nerve-evoked ij.ps. Hyperpolarizations to NO were unaffected by L-NAME, but were blocked by oxyhaemoglobin. 7 Tetrodotoxin, L-NAME and oxyhaemoglobin all caused depolarization of resting membrane potential. 8 The specific guanosine 3':5'-cyclic monophosphate phosphodiesterase inhibitor, M&B 22948, caused hyperpolarization, increased the maximum level of hyperpolarization reached during ij.ps, and increased the duration of ij.ps. 9 These data further support the hypothesis that NANC neurotransmission in the ileocolonic sphincter is mediated by NO or an NO-releasing compound. The data also suggest that tonic release of NO, possibly from spontaneous firing of NANC nerves, may regulate resting membrane potential and tone in this sphincter.

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“…There is purinergic inhibitory neuromuscular transmission in the duodenum and jejunum of most species of laboratory animals [41,91,457,522,620,705,729,730]. Purinergic NANC transmission has been reported in the ileum of pig [158,217] and humans [729,748].…”

Section: Smooth Musclementioning

confidence: 99%

Purinergic signalling in the gastrointestinal tract and related organs in health and disease

Burnstock

2013

Purinergic Signalling

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Purinergic signalling plays major roles in the physiology and pathophysiology of digestive organs. Adenosine 5′-triphosphate (ATP), together with nitric oxide and vasoactive intestinal peptide, is a cotransmitter in nonadrenergic, non-cholinergic inhibitory neuromuscular transmission. P2X and P2Y receptors are widely expressed in myenteric and submucous enteric plexuses and participate in sympathetic transmission and neuromodulation involved in enteric reflex activities, as well as influencing gastric and intestinal epithelial secretion and vascular activities. Involvement of purinergic signalling has been identified in a variety of diseases, including inflammatory bowel disease, ischaemia, diabetes and cancer. Purinergic mechanosensory transduction forms the basis of enteric nociception, where ATP released from mucosal epithelial cells by distension activates nociceptive subepithelial primary afferent sensory fibres expressing P2X3 receptors to send messages to the pain centres in the central nervous system via interneurons in the spinal cord. Purinergic signalling is also involved in salivary gland and bile duct secretion.

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Effect of apamin on the electrical responses of smooth muscle to adenosine 5′-triphosphate and to non-adrenergic, non-cholinergic nerve stimulation

Cited by 128 publications

References 11 publications

Distribution and properties of excitatory and inhibitory junction potentials in circular muscle of the guinea‐pig stomach.

Distribution and properties of excitatory and inhibitory junction potentials in circular muscle of the guinea‐pig stomach.

Role of nitric oxide in non‐adrenergic, non‐cholinergic inhibitory junction potentials in canine ileocolonic sphincter

Purinergic signalling in the gastrointestinal tract and related organs in health and disease

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