• The Korean Journal of Physiology
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• v.10 no.2
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• pp.1-10
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• 1976

The action of acetylcholine on the sodium plus potassium activated ATPase activity in the rabbit red cell membrane has been investigated and the experiments were also designed to determine the mechanism of action of acetylcholine on the ATPase activity. The following results were observed. 1. The activity of the NaK ATPase from red cell membrane is inhibited by acetylcholine. 2. The ratio of inhibition of NaK ATPase by acetylcholine is decreased by raising the potassium concentration, and is increased by raising the sodium concentration. 3. The ATPase activity is increased by small amounts of calcium but inhibited by larger amounts. The ratio of inhibition of the enzyme by acetylcholine is increased by raising the calcium concentration. 4. The inhibitory action of acetylcholine on the NaK ATPase activity was not related to the sulfhydryl group of cysteine, the hydroxyl group of threonine, or the carboxyl group of aspartic acid. 5. The inhibitory action of acetylcholine on the ATPase activity is due to amino group of the enzyme of NaK ATPase.

• The Journal of Internal Korean Medicine
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• v.17 no.1
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• pp.175-192
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• 1996

These studies were carried out to investigate the effect of Jungchuntang water extract on the inhibitory contractile action of acetylcholine in rat. The results of these studies were as follows; 1. Contractile force of acetylcholine from trachea smooth muscle in rat was significantly inhibited by Jungchuntang. 2. Dose-response of acetylcholine pretreated Jungchuntang in rat was not significantly changed. 3. Inhibitory contractile action of acetylcholine pretreated propranolol in rat was decreased. 4. Inhibitory contractile action of acetylcholine pretreated indomethacin was not significantly changed by Jungchuntang. 5. Inhibitory contractile action of acetylcholine pretreated methylene blue was significantly changed by Jungchuntang. 6. Contractile force of acetylcholine from trachea smooth muscle in rat was significantly inhibited by Jungchuntang. 7. Dose-response of acetylcholine pretreated Jungchuntang in rat was not significantly changed. 8. Inhibitory contractile action of acetylcholine pretreated propranolol in rat was decreased. 9. Inhibitory contractile action of acetylcholine pretreated indomethacin was not significantly changed by Jungchuntang. 10. Inhibitory contractile action of acetylcholine pretreated methylene blue was significantly changed by Jungchuntang.

• The Journal of Internal Korean Medicine
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• v.14 no.2
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• pp.1-19
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• 1993

This study was carried out to investigate the effects of Gooboeum extract on the inhibitory contractile action of acetylcholine in the control and sensitized rat. The results were obtained as follows: 1. The acetylcholine contractile force of the trachea smooth muscle with epithelium was significantly relaxed by Gooboeum. 2. Dose-response of acetylcholine from the trachea smooth muscle pretreated Gooboeum was not changed. 3. Effect of Gooboeum on the inhibitory contractile action of trachea smooth muscle pretreated propranolol was not significantly inhibited. 4. The inhibitory contractile action of acetylcholine of trachea smooth muscle pretreated indomethacin was not significantly changed by Gooboeum. 5. Effects of Gooboeum extract on the inhibitory contractile action of acetylcholine of trachea smooth muscle pretreated methylene blue was not significant. 6. The contractile force of acetylcholine of the trachea smooth muscle without epithelium was significantly inhibited by Gooboeum. 7. Dose-response of acetylcholine of the trachea smooth muscle pretreated Gooboeum was not significant. 8. Effects of Gooboeum extract on the inhibitory contractile action of acetylcholine of the trachea smooth muscle pretreated propranolol was significantly inhibited. 9. Effects of Gooboeum extract on the inhibitory contractile action of acetylcholine of the trachea smooth muscle pretreated indomethacin decreased. 10. Effects of Gooboeum extract on the inhibitory contractile action of acetylcholine of the trachea smooth muscle pretreated methylene blue was not significant.

• The Journal of Internal Korean Medicine
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• v.15 no.2
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• pp.240-248
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• 1994

These studies were carried out to investigate the effects of Macmundongtang extract on the inhibitory contractile action of acetylcholine in control rat. The results of these studies were as follows: 1. Contractile force of acetylcholine from tracheal smooth muscle in control rat was significantly inhibited by Macmundongtang. 2. Inhibition contractile action of acetylcholine pretreated ACH $ED_{50}$ in control rat was significantly changed. 3. Dose-response of acetylcholine pretreated Macmundongtang in control rat was not significant. 4. Inhibitory contractile action of acetylcholine pretreated propranolol in control rat was not significantly changed by Macmundongtang. 5. Inhibitory contractile action of acetylcholine pretreated methylene blue in control rat was significantly changed. 6. Contractile force of acetylcholine pretreated indomethacin from trachea smooth muscle in control rat was not significantly inhibited by Macmundongtang.

• Archives of Pharmacal Research
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• v.19 no.6
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• pp.520-528
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• 1996

The involvement of the cyclic AMP (cAMP) effector system in the release of endogenous dopamine and acetylcholine from the rat neostriatum was assessed. Forskolin, an activator of adenylate cyclase, was used to enhance cAMP production, and the consequence of this enhancement on the spontaneous and potassium stimulated release of dopamine and acetylcholine was evaluated. Neostriatal slices were prepared from Fischer 344 rats and after a preincubation period the release of each endogenous neurotransmitter was measured from the same slice preparation. To measure acetylcholine release the slice acetylcholinesterase (AChE) activity was inhibited with physostigmine, but the release from slices with intact AChE activity was also determined (choline, instead of acetylcholine was detected in the medium). Under both conditions forskolin induced a significant dose-dependent increase in the potassium-evoked release of dopamine. In the same tissue preparations the release of neither acetylcholine (AChE inhibited) nor choline (AChE intact) was affected by forskolin. The results indicate that the CAMP second messenger system might be involved in neuronal mechanisms that enhance neostriatal dopamine release, but stimulation of this second messenger by forskolin does not further enhance neostriatal acetylcholine release.

• The Journal of Internal Korean Medicine
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• v.15 no.1
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• pp.227-237
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• 1994

These studies were carried out to investigate the effects of Ohotang water extract on the inhibitory contractile action of acetylcholine in control rat. The results of these were as follows; 1. Contractile force of acetylcholine from trachea smooth muscle in control rat was significantly inhibited by Ohotang. 2. Dose-response of acetylcholine pretreated Ohotang in control rat was significantly inhibited. 3. Inhibitory contractile action of acetylcholine pretreated propranolol in control rat was significantly inhibited by Ohotang. 4. Contractile force of acetylcholine pretreated indomethacin from trachea smooth muscle in control rat was not significantly changed. 5. Inhibitory contractile action of acetylcholine pretreated methylene blue in control rat was not significantly changed.

• The Journal of Internal Korean Medicine
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• v.15 no.1
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• pp.138-151
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• 1994

These studies were carried out to investigate the effect of Onpaetang water extract on the inhibitory contractile action of acetylcholine in sensitized rat. The results of these studies were as follows; 1. Contractile force of acetylcholine from trachea smooth muscle in sensitized rat was significantly inhibited by Onpaetang. 2. Dose-response of acetylcholine pretreated Onpaetang in sensitized rat was not significantly changed. 3. Inhibitory contractile action of acetylcholine pretreated propranolol in sensitized rat was decreased. 4. Inhibitory contractile action of acetylcholine pretreated indomethacin was not significantly changed by Onpaetang. 5. Inhibitory contractile action of acetylcholine pretreated methylene blue was not significantly changed by Onpaetang. 6. Inhibitory contractile action of acetylcholine pretreated tetrodotoxin was not significantly changed by Onpaetang.

• The Korean Journal of Pharmacology
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• v.3 no.1
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• pp.51-55
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• 1967

A few reports suggested that guanidine increases the quantity of acetylcholine released from the nerve endings and increases the sensitivity of the end plate to acetylcholine. In this experiment the authors attempted to investigate the influence of guanidine on the acetylcholine effect on the blood pressure of rabbits and excised intestine. The results obtained we re summarized as follows. 1. The hypotensive effect of acetylcholine on the rabbit is augmented by pretreatment with guanidine 5-10 mg/kg. however is inhibited by 20 mg/kg of guanidine. 2. The contractile effect of acetylcholine on the excised intestine of rabbit and rat is potentiated by guanidine.

• The Korean Journal of Pharmacology
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• v.27 no.2
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• pp.125-133
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• 1991

In the isolated rabbit mesenteric artery denuded of endothelium, we characterized the identity of the A23187-induced endothelium-dependent relaxing factor (EDRF) released from the endothelium of rabbit aorta, which is distinct from that of acetylcholine-induced relaxing factor. In the normal physiological salt solution (PSS), the dose-response curves to A23187 and acetylcholine were overlapped together. Their effects were also inhibited by methylene blue. Upon application of hypoxanthine and xanthine oxidase into the bath, the phenylephrine-induced precontraction was transiently increased followed by the sustained relaxation. During the burst of hypoxanthine-xanthine oxidase reaction, the $Ca^{++}$ ionophore, A23187 but not acetylcholine was able to cause an immediate relaxation. However, A23187-induced relaxation was not manifested when precontracted by 50 mM $K^+-PSS$. Nevertheless, in the presence of superoxide dismutase, A23187 could produce an immediate relaxation without accompanying the transient contraction as acetylcholine did during the hypoxanthine-xanthine oxidase reaction. On the other hand, acetylcholine-induced relaxation was more sensitively inhibited by phorbol 12-myristate 13-acetate (PMA) than A23187-induced relaxation. Endothelium-independent relaxation to sodium nitroprusside was not affected by PMA. Based on these results it is suggested that both A23187 and acetylcholine cause the methylene blue-inhibitable endothelium-dependent relaxation, and in addition, A23187 may release a stable EDRF which is resistant to superoxide anion and PMA.

• Journal of Acupuncture Research
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• v.23 no.3
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• pp.117-127
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• 2006

Alzheimer's disease (AD) is the most prevalent form of neurodegenerative disease associated with aging in the human population. This disease is characterized by the following 4 structural changes : Atrophy of the Cortex, Parasympathetic, and other neural cells, the existence of Neurofibrillary tangles (NFTs), and the accumulation of Senile plaques. NFTs and Senile plaques is known to be the index of this disease. Senile plaques disturbs the neutro transmission and depletes of Acetylcholine. So, Recovery of Acetylcholine is the primal objective for treating Alzheimer's disease. So, Inhibiting the activity of Acetylcholine Esterase (AChE), which causes the hydrolysus of acetylcholine into choline and acetate, can be seen as a key role for treating Alzheimer's disease. Increasing body of evidence has been demonstrated that Bee Venom Acupuncture (BV) could compete with complex protein involving in multiple step of $NF-_{\kappa}B$ activation and exert the anti-inflammatory potential of combined inhibition of the prostanoid and nitric oxide synthesis systems by inhibition of IKK and $NF-_{\kappa}B$. BV dose-dependently attenuated Scopolamine-induced Acetylcholine esterase activities in cerebral cortex and hippocampus of the mice brain. This study therefore suggests that BV acupuncture method may be useful for prevention of development or progression of AD.