Histamine H3 receptor-mediated inhibition of endogenous acetylcholine release from the isolated, vascularly perfused rat stomach

Yokotani, Kunihiko; Murakami, Yoshinori; Okada, Shoshiro; Wang, Muchun; Nakamura, Kumiko

doi:10.1016/s0014-2999(00)00085-6

Cited by 22 publications

(21 citation statements)

References 27 publications

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“…Our data are consistent with this hypothesis. In contrast, others reported that muscarinic receptors inhibit catecholamine release from sympathetic nerves (Lavallée et al, 1978;Muscholl, 1980) due to activation of M 2 cholinoceptors (Yokitani and Osumi, 1993). This would be expected to produce the opposite effects as those seen in our study.…”

Section: Discussioncontrasting

confidence: 96%

Muscarinic Cholinergic and β-Adrenergic Contribution to Hindquarters Vasodilation and Cardiac Responses to Cocaine

Knuepfer

2003

J Pharmacol Exp Ther

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Cocaine produces a pressor response associated with an initial hindquarters vasoconstriction followed by a prolonged vasodilation in conscious rats. Propranolol pretreatment prevented the vasodilation and enhanced the pressor response, whereas atropine methylbromide pretreatment reduced the increase in systemic vascular resistance. We studied the role of selective muscarinic and ␤-adrenoceptor antagonists on responses to cocaine in rats with an increase in systemic vascular resistance to cocaine (vascular responders). Arterial blood pressure and ascending aortic and distal descending aortic blood flow using pulsed Doppler flowmetry were measured. In conscious rats, cocaine (5 mg/kg i.v.) elicited consistent pressor responses but variable systemic and hindquarters vascular resistance responses that were directly correlated, suggesting that skeletal muscle resistance responses comprise an important component of systemic vascular resistance. ICI 118,551 [(Ϯ)-1-[2,3-(dihydro-7-methyl-1H-inden-4-yl)oxy]-3-[(1-methylethyl)-amino]-2-butanol] (0.5 mg/kg i.v.) pretreatment prevented the hindquarters vasodilation, enhancing the increase in systemic vascular resistance and the pressor response while further depressing the cardiac output response, similar to the effects of propranolol. Atenolol (1 mg/kg) pretreatment attenuated the stroke volume and cardiac output responses while enhancing the increase in systemic vascular resistance without affecting the hindquarters responses. In contrast, M 2 antagonist methoctramine (0.3 mg/kg) pretreatment had similar effects as atropine in reducing the decrease in cardiac output by reducing the increase in systemic vascular resistance, whereas the M 1 antagonist pirenzipine (0.02 mg/kg) did not alter responses. Therefore, the cocaine-induced pressor response is ameliorated by ␤ 2 -adrenoceptor mediated skeletal muscle vasodilation, whereas the decrease in cardiac output and the increase in systemic vascular resistance are dependent on M 2 -cholinoceptor activation.

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Section: Discussioncontrasting

confidence: 96%

Muscarinic Cholinergic and β-Adrenergic Contribution to Hindquarters Vasodilation and Cardiac Responses to Cocaine

Knuepfer

2003

J Pharmacol Exp Ther

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“…This increase may be due in part to inhibition of neuronal M 2 muscarinic receptors. M 2 muscarinic receptors have been localized to sympathetic nerves where they limit noradrenaline release (Racke et al, 1992;Yokotani and Osumi, 1993;Lambrecht et al, 1999). Thus, inhibition of M 2 muscarinic receptor function by insulin would lead to increased noradrenaline release.…”

Section: Discussionmentioning

confidence: 99%

Insulin Regulates Neuronal M₂Muscarinic Receptor Function in the Ileum of Diabetic Rats

Coulson

Jacoby

Fryer

2003

J Pharmacol Exp Ther

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Acetylcholine release from cholinergic nerves in the gastrointestinal tract is limited by neuronal M 2 muscarinic receptors. In diabetic animals, M 2 muscarinic receptor function in the ileum is increased, leading to decreased acetylcholine release and smooth muscle contraction in response to nerve stimulation. The mechanisms responsible for increased M 2 muscarinic receptor function are unknown but may contribute to the gastrointestinal dysmotility that occurs frequently in diabetics. In this study, we investigated whether insulin modulates M 2 muscarinic receptor function in the gastrointestinal tract of diabetic rats. M 2 muscarinic receptor function was tested by measuring the ability of an agonist, pilocarpine, to inhibit and an antagonist, methoctramine, to potentiate electrical field stimulation (EFS)-induced contraction of ileum in vitro. Insulin administration (0.2, 0.6, and 2 U s.c. daily for 7 days) reversed the diabetes-induced increase in M 2 muscarinic receptor function and restored normal contractions to EFS. Insulin had no effect on the function of postjunctional M 3 muscarinic receptors, determined by measuring contractile responses to acetylcholine. These data suggest that insulin tonically inhibits neuronal M 2 muscarinic receptors. Thus, loss of insulin removes this inhibition and increases M 2 muscarinic receptor function leading to decreased acetylcholine release and contraction to EFS. In nondiabetic rats, there was a trend that higher insulin doses (0.6 and 2 U) increased M 2 muscarinic receptor function, suggesting a bell-shaped concentration-response relationship for insulin. In conclusion, lack of insulin or excess insulin increases M 2 muscarinic receptor function in rat ileum. This mechanism may contribute to decreased acetylcholine release in the gastrointestinal tract of diabetics, resulting in dysmotility.

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“…Pertussis toxin has been shown to ADP-ribosylate the a subunit of some GTP-binding proteins (G i or G o ), resulting in their inactivation (37,38). Since the pretreatment with pertussis toxin (10 m g/ rat, for 4 days) abolished the negative chronotropic and inotropic effects of oxotremorine (a muscarinic receptor agonist) on the isolated, spontaneously beating rat atria preparation (24), pretreatment with the same dose of this toxin seems to be enough to block pertussis toxin-sensitive GTP-binding proteins in the rat stomach. In the present experiment, endothelin-1-induced inhibition of the evoked release of noradrenaline was attenuated by pertussis toxin, suggesting the involvement of these toxin-sensitive GTP-binding proteins in the endothelin ET A receptor-mediated inhibition of noradrenaline release from the gastric sympathetic nerve terminals.…”

Section: Discussionmentioning

confidence: 99%

“…In some experiments, rats were pretreated with pertussis toxin (10 m g per rat dissolved in 0.1 ml of sodium phosphate-buffered saline, pH 7.0, 4 days before experiments) or vehicle injected into the dorsal penic vein under a light ether anesthesia, as described in our previous paper (24).…”

Section: Perfusion Experimentsmentioning

confidence: 99%

Endothelin ETA- and ETB-Receptor-Mediated Inhibition of Noradrenaline Release From Isolated Rat Stomach

Nakamura

Okada²,

Yokotani³

2003

J Pharmacol Sci

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Abstract. We examined the effect of endothelin-1, endothelin-3 and sarafotoxin S6c on the release of noradrenaline from gastric sympathetic nerve terminals using an isolated, vascularly perfused rat stomach. The release of noradrenaline evoked by electrical stimulation of the gastric postganglionic sympathetic nerves (at 2.5 Hz for 1 min) was inhibited by endothelin-1 (10 -10 -10 -8 M), endothelin-3 (10 -9 -10 -8 M) and sarafotoxin S6c (a highly selective agonist of endothelin ET B receptors) (10 -9 -10 -8 M) in a concentration-dependent manner; the inhibitory potencies were as follows: endothelin-1 > endothelin-3 > sarafotoxin S6c. The inhibitory effect of endothelin-1 (3´10 -9 M) on noradrenaline release was abolished by BQ-123 (a selective antagonist of endothelin ET A receptors) in a dose-dependent manner (10 -7 and 10 -6 M), but not influenced by BQ-788 (a selective antagonist of endothelin ET B receptors) (10 -7 and 10 -6 M). The endothelin-1-induced inhibition of noradrenaline release was attenuated by pretreatment with pertussis toxin (10 m g/animal, i.v., 4 days before experiments), but not influenced by indomethacin (3´10 -6 M). These results indicate that endothelin ET A and ET B receptors located on the sympathetic nerve terminals play a role in the inhibition of noradrenaline release from the rat stomach: endothelin ET A receptor-mediated inhibition is carried out by pertussis toxin-sensitive and indomethacininsensitive mechanisms.

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Histamine H3 receptor-mediated inhibition of endogenous acetylcholine release from the isolated, vascularly perfused rat stomach

Cited by 22 publications

References 27 publications

Muscarinic Cholinergic and β-Adrenergic Contribution to Hindquarters Vasodilation and Cardiac Responses to Cocaine

Muscarinic Cholinergic and β-Adrenergic Contribution to Hindquarters Vasodilation and Cardiac Responses to Cocaine

Insulin Regulates Neuronal M₂Muscarinic Receptor Function in the Ileum of Diabetic Rats

Endothelin ETA- and ETB-Receptor-Mediated Inhibition of Noradrenaline Release From Isolated Rat Stomach

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Histamine H3 receptor-mediated inhibition of endogenous acetylcholine release from the isolated, vascularly perfused rat stomach

Cited by 22 publications

References 27 publications

Muscarinic Cholinergic and β-Adrenergic Contribution to Hindquarters Vasodilation and Cardiac Responses to Cocaine

Muscarinic Cholinergic and β-Adrenergic Contribution to Hindquarters Vasodilation and Cardiac Responses to Cocaine

Insulin Regulates Neuronal M2Muscarinic Receptor Function in the Ileum of Diabetic Rats

Endothelin ETA- and ETB-Receptor-Mediated Inhibition of Noradrenaline Release From Isolated Rat Stomach

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Insulin Regulates Neuronal M₂Muscarinic Receptor Function in the Ileum of Diabetic Rats