The effect of apamin on the smooth muscle cells of the guinea-pig taenia coli

Maas, Ad J.J.; Hertog, Adriaan den

doi:10.1016/0014-2999(79)90006-2

Cited by 108 publications

(45 citation statements)

References 12 publications

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“…The hyperpolarization of taenia coli evoked by this procedure is blocked by apamin (Shuba & Vladimirova, 1980;Maas & den Hertog, 1979;Mackenzie & Burnstock 1980;Maas, 1981). It has also been shown that the ATP-induced hyperpolarization is abolished by apamin (Shuba & Vladimirova, 1980;Maas & den Hertog, 1979;Mackenzie & Burnstock, 1980;Maas, den Hertog, Ras & den Akker, 1980;Brown & Burnstock, 1981). The latter observation is at variance with the findings of this study (Figs.…”

Section: Discussionsupporting

confidence: 47%

“…Apamin has also been shown to block the a-adrenergic relaxation of taenia coli (Banks, Brown, Burgess, Burnstock, Claret, Cocks & Jenkinson, 1979;Maas & den Hertog, 1979;Muller & Baer, 1980) although not in a competive manner (Jenkinson, 1981). An a-blocking effect was also noted in this study during the first 10 min after giving apamin by close I.A.…”

Section: Discussionmentioning

confidence: 99%

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The effect of apamin on non‐adrenergic, non‐cholinergic vasodilator mechanisms in the intestines of the cat.

Jodal¹,

Lundgren²,

Sjöqvist³

1983

The Journal of Physiology

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SUMMARY1. The effects of apamin, a polypeptide isolated from bee venom, on different vasodilator mechanisms in the small and large intestines were studied in atropinized cats.2. In the large intestine vasodilatation in response to pelvic nerve stimulation was either abolished or markedly diminished by I.A. apamin. However, neither the contraction of colonic muscle which occurred under these conditions nor sympathetic vasoconstriction was significantly influenced by apamin, suggesting that the effect of the peptide was not a non-specific effect on nerves or vascular smooth muscle.3. In the small intestine it was observed that the nervous vasodilatation induced by transmural electrical field stimulation or mechanical mucosal stimulation was either diminished or abolished by apamin.4. Intestinal vasodilatation, caused by close I.A. infusions of 5-hydroxytryptamine (5-HT), was abolished by apamin. After giving apamin 5-HT infusions induced a vasoconstriction in five out of six experiments.5. Vasodilatation induced by vasoactive intestinal polypeptide (VIP) was not significantly affected by apamin.6. In a series of in vitro experiments on rat portal vein, dose--response curves of several putative intestinal neurotransmitters were determined in the presence and absence of apamin. The following substances were tested: VIP, substance P, bradykinin, 5-HT, ATP and adenosine. Apamin had no effect on the dose-response curves of any of these compounds.7. The results are discussed in relation to the possibility that apamin may act by blocking the release of a putative peptidergic transmitter from nerve terminals.

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Section: Discussionsupporting

confidence: 47%

Section: Discussionmentioning

confidence: 99%

The effect of apamin on non‐adrenergic, non‐cholinergic vasodilator mechanisms in the intestines of the cat.

Jodal¹,

Lundgren²,

Sjöqvist³

1983

The Journal of Physiology

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“…Thus, in both cases a hyperpolarization of the smooth muscle membrane is induced together with a rapid, transient relaxation (Bennett et al, 1966;Burnstock, 1979;Cocks & Burnstock, 1979;Hills et al, 1983). The bee venom apamin, a presumed potassium-channel blocker, has been shown to reverse the hyperpolarization evoked by exogenously applied ATP to a depolarization in the taenia coli (Maas & den Hertog, 1979). As the hyperpolarization caused by field stimulation was not blocked completely by apamin (Maas & den Hertog, 1979), the residual hyperpolarization could be due to the existence of an additional neurotransmitter other than ATP.…”

Section: Discussionmentioning

confidence: 99%

“…The bee venom apamin, a presumed potassium-channel blocker, has been shown to reverse the hyperpolarization evoked by exogenously applied ATP to a depolarization in the taenia coli (Maas & den Hertog, 1979). As the hyperpolarization caused by field stimulation was not blocked completely by apamin (Maas & den Hertog, 1979), the residual hyperpolarization could be due to the existence of an additional neurotransmitter other than ATP. VIP has also been suggested as a neurotransmitter in the guinea-pig taenia coli (Grider et al, 1985), and could be responsible for the apamin-insensitive part of the response to field stimulation (Mackenzie & Burnstock, 1980;Hills et al, 1983;Costa et al, 1986).…”

Section: Discussionmentioning

confidence: 99%

A possible role of the L‐arginine‐nitric oxide pathway in the modulation of cholinergic transmission in the guinea‐pig taenia coli

Knudsen

Tøttrup

1992

British J Pharmacology

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1 The role of the L-arginine-nitric oxide (NO) pathway for non-adrenergic, non-cholinergic (NANC) relaxation of the guinea-pig taenia coli was studied by recording isometric tension in response to transmural field stimulation (TMS). inhibited these effects of L-NNA. L-NNA (l0-4 M) had no effect on the inhibitory response during TMS in strips preincubated with atropine (10-6M). 6 In conclusion, the L-arginine-NO pathway seems to play a role in the NANC innervation of the guinea-pig taenia coli. The inhibitory effect of NO or a NO-like compound depends on the integrity of the cholinergic pathways and it is proposed that this compound exerts its effects prejunctionally on cholinergic nerves, by inhibiting the release of acetylcholine.

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“…This channel may be responsible for the generation of after-hyperpolarization in some nerves (Romey et al, 1984). In some types of visceral smooth muscle this toxin reversed the ATP-induced hyperpolarization to depolarization or blocked inhibitory junction potentials (Vladimirova & Shuba, 1978;Banks et al, 1979;Maas & Den Hertog, 1979;Komori & Suzuki, 1986), whereas such effects were not found in other muscles (Nakao et al, 1986;Lydrup, 1991). The lack of a direct contractile action of apamin has been observed in many kinds of smooth muscles (Allen et al, 1986;Winquist et al, 1989;Fujii et al, 1990), although contraction is initiated in a few tissues (e.g.…”

Section: Introductionmentioning

confidence: 99%

Modification by charybdotoxin and apamin of spontaneous electrical and mechanical activity of the circular smooth muscle of the guinea‐pig stomach

Suzuki

Ito

Minayoshi

et al. 1993

British J Pharmacology

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1 The effects of charybdotoxin and apamin, putative blockers of Ca2'-activated K+ channels, on spontaneous electrical and mechanical activity of circular smooth muscle of the guinea-pig stomach antrum were examined in the presence of 1 gM tetrodotoxin and I tLM atropine.2 Both charybdotoxin (>3 nM) and apamin (>3 nM) dose-dependently increased the amplitude of spontaneous contractions without altering their frequency. The maximum effect of charybdotoxin was much greater than that of apamin. Both toxins increased the amplitude of intracellular Ca2+ oscillations measured with fura-2.3 When the extracellular Ca2" concentration was lowered to 1.5 mM or less, apamin did not significantly potentiate the contractions whereas charybdotoxin still potentiated them but with less potency.4 Charybdotoxin (30 nM) increased the amplitude of spikes and slow waves, and slightly decreased the resting membrane potential. On the other hand, apamin (100 nM) preferentially increased the slow wave amplitude with no effect on the resting membrane potential. 5 These results suggest that both toxins affect the spontaneous contraction by modifying the electrical activity and that charybdotoxin-sensitive K+ channels and apamin-sensitive ones are differently involved in the spontaneous electrical activity.

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The effect of apamin on the smooth muscle cells of the guinea-pig taenia coli

Cited by 108 publications

References 12 publications

The effect of apamin on non‐adrenergic, non‐cholinergic vasodilator mechanisms in the intestines of the cat.

The effect of apamin on non‐adrenergic, non‐cholinergic vasodilator mechanisms in the intestines of the cat.

A possible role of the L‐arginine‐nitric oxide pathway in the modulation of cholinergic transmission in the guinea‐pig taenia coli

Modification by charybdotoxin and apamin of spontaneous electrical and mechanical activity of the circular smooth muscle of the guinea‐pig stomach

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