• Journal of Ginseng Research
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• v.17 no.2
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• pp.109-113
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• 1993

The effects of ginseng total saponins (GTS) on the action of U-50,488H, a $textsc{k}$-opioid receptor agonist, on the electrically induced twitch responses of mouse vats deferens were studied. U-50,488H ($10^9$~$10^{-5}$M) inhibited the twitch contractions in a dose-dependent manner, which were caused by adenosine 5'-triphosphate (ATP) released from the stimulated sympathetic nerve, and this effect was antagonized by naloxone ($10^6$ M). GTS, which itself induced the inhibition of the twitch contractions, acted additively to U-50,488H, GTS and U-50,488H had no effect on the tension of the unstimulated organs. The contractions elicited by ATP were not affected by U-50,488H, but inhibited by GTS. These results suggest that U-50,488H suppressed the twitch contractions by the inhibition of neurotransmitter release from presynaptic nerve terminals via action on opioid receptor, but G75, by inhibiting the action of the neurotransmitter on the smooth muscle.

• Korean Journal of Veterinary Service
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• v.17 no.3
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• pp.255-263
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• 1994

To elucidate the action of the adrenergic nerve on the isolated uterine smooth muscle of the pig, effects of electrical transmural nerve stimulation and norepinephrine were investigated on the pretreatment of phentolamine ； non-selective ${\alpha}$-adrenoceptor blocker, propranolol ; ${\beta}$-adrenoceptor blocker and the yohimbine；${\alpha}_2$-selective adrenoceptor blocker from physiograph. 1. The relaxation response induced by norepinephrine was the concentration of $10^{-6}$ M at first and maximum response was concentration of $10^{-4}$M. 2. The relaxation response induced by norepinephrine was not effected by the pretreatment with non-selective $\alpha$-adrenoceptor blocker, phentolanune ($10^{-6}$ M) but was completely blocked by the pretreatment with ${\beta}$-adrenoceptor blocker, propranolol($10^{-6}$ M). 3. The contractile response induced by electrical transmural nerve stimulation(20V, 10Hz, 0.5msec, 20sec ) was inhibited by the pretreatment with non-selective ${\alpha}$-adrenoceptor blocker, phentolamine($10^{-6}$ M) but was not inhibited and rather increased by the pretreatment ${\beta}$-adrenoceptor blocker, propranolol($10^{-6}$ M), and was not approximately effected by the pretreatment with ${\alpha}_2$-adrenoceptor blocker, yohimbine($10^{-6}$ M). These finding suggest that it was excitatory action by ${\alpha}_1$-adrenergic nerve and inhibitory action by ${\alpha}_2$-adrenergic, ${\beta}$-adrenergic nerve on uterine smooth muscle of the pig.

• Journal of Pharmaceutical Investigation
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• v.14 no.2
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• pp.92-103
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• 1984

The action of debrisoquine on renal function in rabbits was studied. 1. When debrisoquine was given into ear vein, it did not affect on renal functin with smaller doses of 0.1 or 0.3mg/kg, while with higher dose of 1.0mg/kg it elicited the significant decrease of urine flow, renal plasma flow and glomerular filtration rate, and the increase of filtration fraction, and at the same time sodium excreted in urine, FENa (fractional excretion of sodium) and osmolar clearance were significantly decreased, and then it exhibited the increase of $K^+/Na^+$ ratio and no changes of $T^cH_2O$. 2. Debrisoquine (1.0mg/kg), when injected repeatedly into a vein, produced a more marked decrease of urine flow. 3. Debrisoquine induced-antidiuretic action was not affected by pretreatment with phentolamine (2mg/kg, i.v.), alpha-sympathetic blocking agent. 4. Debrisoquine given intracerebroventricularly did not produce a significant change on renal function in dose of 0.1mg/kg. These results suggest that debrisoquine produce the antidiuretic effect in rabbit, and the mechanism of its action is due to dual actions that are the decrease of hemodynamic effect and the facilitation of reabsorption of sodium in renal tubules.

• The Korean Journal of Pharmacology
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• v.14 no.1_2
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• pp.55-62
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• 1978

Ban formulated the concept of 'sympathetic center' and 'parasympathetic center' in the central nervous system, and Folkow et al. reported that the electric stimulation of the posterior part of hypothalamus induced the marked liberation of catecholamines from the adrenal medulla. Tatum reported that the hyperglycemic action of picrotoxin is contributed to the cathecholamines liberation from adrenal medulla by the excitation of hypothalamus via splanchnic nervous plexus. In this paper, the relationship between the convulsive action and the hyperglycemic effect of picrotoxin was investigated, with references to the influences of several drugs related with adrenergic function and two intravenous anesthetics on the picrotoxin hyperglycemia. The results obtained were summarized as follows; 1) There was no difference between the convulsive dose(1. 5mg/kg) and the subconvulsive dose (0.75mg/kg) of picrotoxin in its hyperglycemic effect that was not affected with the phenobarbital pretreatment, but the efficacy of its hyperglycemic action was more prominent than that of strychnine. 2) The hyperglycemic effect of picrotoxin was markedly suppressed by the pretreatment of thiopental or ketamine. 3) The hyperglycemic effect was not affected by the reserpine pretreatment, but the effect was markedly suppressed by the pretreatment of iproniazid or chlorpromazine. 4) The hyperglycemic effect of picrotoxin was significantly suppressed by the pretreatment of hexamethonium, propranolol or guanethidine, and the order of those suppressing efficacy was propranolol> hexamethonium> guanethidine.

• YAKHAK HOEJI
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• v.31 no.6
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• pp.376-393
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• 1987

This study was performed in order to investigate the effect of nifedipine, a vasodilating drug which acts through calcium antagonism, on renal function using mongrel dog. Nifedipine, when given interavenously in doses ranging from 1.5 to 5.0$\mu\textrm{g}$/kg, elicited diuresis along with less changes of glomerular filtration rate and significant increases of renal plasma flow, so that the filtration fraction(FF) decreased significantly, at the same time both osmolar and free water clearances increased, and amount of sodium, potassium and calcium excreted in urine increased significantly. Nifedipine, when infused into a renal artery in doses from 0.05 to 0.15$\mu\textrm{g}$/kg/min, exhibited identical responses to the actions of intraveneous nifedipine except significant increase of glomerular filtration rate and no change of FF, which was confined only to the infused kidney. The renal action of nifedipine into a renal artery were not influenced by renal denervation, decreased significantly by ouabain, Na$^+$-K$^+$-ATPase inhibitor, which was given into a renal artery. Nifedipine infused into a renal artery in dog pretreated with propranolol i.v. produced diuresis associated with the increase of electrolytes excretion by reduction of electrolyte reabsorption and with no changes of glomerular filtration rate and renal plasma flow. Thus, it is concluded that nifedipine infused into a renal aretery produces diuretic action along with both improvement of hemodynamics and inhibition of electrolytes reabsorption, which may be related to sympathetic $\beta$-receptor or Na$^+$-K$^+$-ATPase activity because the action of nifedipine in kidney is blocked by propranolol or ouabain.

• Journal of the Korean Society of Food Science and Nutrition
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• v.14 no.3
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• pp.253-258
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• 1985

It was aimed to elucidate the underlying mechanism which is elevated the systemic arterial blood pressure by cadmium(Cd). By using the isolated vas deferens and tail artery from Cd-poisoned rats, it was undertaken to see whether the ${\alpha}-adrenoceptor$ activity and prostaglandins action on the twitch response to electrical stimulation were altered. It was discussed in relation with sympathetic nerve activity. The response to electrical stimulation in vas deferens from Cd-poisoned rats was much enhanced, and frequency 50(Freq.50) was significantly lowered, comparing to control. However, the response of rat tail artery was attenuated by Cd. Inhibitory action of clonidine on the twitch response of vas deferens to electrical stimulation was decreased by Cd-poisoning. However, the increase in response in the presence of methoxamine was not affected. The inhibitory action of prostaglandin $E_2$ on the twitch response in the vas deferens but not in the tail artery was abolished or rather inverted by Cd-poisoning. In the tail artery from Cd-poisoned rats, the maximum contraction to methoxamine or clonidine was significantly decreased, however, $ED_{50}$ of both agonists was not changed. These results suggest that in vas deferens the autoreceptor of presynaptic membrane is inhibited by Cd-poisoning, by which mechanism the sympathetic activity is being enhanced and this alteration may be causally related to the elevation of arterial pressure.

• The Korean Journal of Pain
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• v.12 no.2
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• pp.242-245
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• 1999

Gabapentin is an oral antiepileptic agent with an unknown mechanism of action. There have been many proposed uses for gabapentin, including neuropathic pain, reflex sympathetic dystrophy, postherpetic neuralgia, midscapular pain secondary to radiation myelopathy and migraine prophylaxis. This report presents patients who were treated with gabapentin when other pharmacologic interventions failed to relieve neuropathic pain 3 patients with neuropathic pain were included among these cases. All patients were started on 200 mg gabapentin. The maximum dose required for pain relief was between 800 mg and 2400 mg. Gabapentin may be a useful adjunct for treating neuropathic pain with minimum of side effects.

• YAKHAK HOEJI
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• v.30 no.3
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• pp.111-120
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• 1986

The influence of debrisoquine on pressor actions of norepinephrine (NE) and tyramine (TR) was investigated in rabbits. Debrisquine(D), in the doses of 1.0, 3.0 and 6.0.mu.g/kg, i.v. potentiated significantly the pressor actions of NE and TR, except the action of TR in the dose of 1.0mg/kg of debrisoquine. NE response potentiated by debrisoquine was not affected by tranylcypromine, a MAO inhabiter, or desipramine, a NE uptake blocking agent, but augmented by reserpine, a NE depleting agent, or bethanidine, a sympathetic neuronal blocking agent. NE response potentiated by tranylcypromine or desipramine was augmented by debrisoquine, while NE response potentiated by reserine or bethanidine was not affected by debrisoquine. TR response potentiated by debrisoquine was weakened by tranylcypromine, desipramine or reserpine, and not affected by bethanidine. TR response in rabbit pretreated with tranylcypromine, desipramine or reserpine was augmented by debrisoquine, but in rabbit pretreated with bethanidine was not affected by debrisoquine.

• The Korean Journal of Pharmacology
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• v.8 no.2
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• pp.35-39
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• 1972

Previous studies on the effect of the visible lights on the organism have shown the possible influences on the nervous system. It was reported that the illumination of blue beam increased the sympathetic tone and that of red beam increased the parasympathetic tone. The pharmacological actions of the sympathomimetics were also known to be altered by various visible lights. But their modes and mechanisms of actions on the nervous system have not been clarified and is obscure. To elucidate the precise mechanism of action of the visible lights on the nervous system, present study was made to observe the survival time of the mole living in the dark environment, under the illumination of the various visible lights and influences of several drugs. The results are summerized as follows: 1. The illumination of the natural sun light caused the survival time of the mole to be shortened and visible monochromatic beams (red, blue and green) even more markedly shortened the survival time. No significant difference was noted depending on the wave length of the chromatic beam. 2. The shortened survival time caused by the visible monochromatic lights was prolonged by strychnine but not affected by morphine. 3. The survival time under the illumination of the visible monochromatic lights was prolonged by acetylcholine and physostigmine. 4. The shortened survival time under the illumination of the monochromatic visible lights was not affected by adrenaline but prolonged by priscoline. It is suggested that the shortened survival time of the mole by the illumination of the visible lights can be prolonged by the stimulation of central and parasympathetic nervous system and blocking of the sympathetic nervous system.

• The Journal of the Korea Contents Association
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• v.21 no.6
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• pp.128-137
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• 2021

The purpose of this study is to examine the effect of sympathetic reactions to public service advertisement video messages produced for health campaigns. To this end, based on the empathy response scale proposed by Campbell & Babrow (2004), the empathy response to the images of nine health campaigns with themes of smoking cessation, tuberculosis, and suicide triggered fear of health risks and health behaviors (information seeking, preventive actions). As a result of the analysis, among the factors of empathy reaction, the reality of the message creative, the match of emotions, and the identification of the characters in the video each played a role in raising fear, and it is rather fear that logically understanding the situation that causes health problems through the health campaign video It was found that it played a role in reducing health information seeking behavior. On the other hand, it was found that the higher the degree of interest, such as sympathy for the characters in the video, among the factors of the sympathetic response to the health campaign, the higher the intention of preventive action to reduce the health risk.