• The Korean Journal of Applied Statistics
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• v.33 no.6
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• pp.823-832
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• 2020

The analgesic effects of music in people with glasses on perceived pain through cold-pressor task (CPT) is assessed based on three-sequence, three-period, crossover trial with three treatment conditions(music-listening, news-listening, and no-sound) to each subject. Fifty subjects are divided into three sequence groups by randomization, and CPTs under the pre-assigned treatment conditions at each period are performed. Pain responses after each CPT, subjects' pain tolerance (PT) in time scale and pain intensity (PI) and pain unpleasantness (PU) in visual analog scale (VAS) are measured. After classifying the group by whether or not to wear glasses, which is the phenotype of the myopia gene, pain responses are compared by F-tests and Tukey's multiple comparisons. CPT pain responses in group with glasses during the music intervention are significantly different from responses during the news intervention and the control conditions, respectively. This study investigates the pain responses of music intervention in the group wearing glasses, which can be seen as a phenotype of the nearsighted gene, and this result would play a role in explaining the biopsychosocial model of the pain mechanism.

• YAKHAK HOEJI
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• v.21 no.1
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• pp.17-25
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• 1977

Intravenous injection of Mori Radicis Cortex Water Extract (MWE) regularly caused the does-related, lowering of blood pressure in the rabbits anesthetized with urethane, and then did not show the cumulative effect and the tachyphylaxis. The hypotensive effects of MWE were inhibited by atropine, chlorisodamine, phentolamine and bethanidine, while not altered by diphenhydramine, propranolol and cyproheptadine. Atropine after chlorisondamine did not alter the effect of MWE. MWE potentiated the pressor effect of nore-pinephrine, but did not carotid occlusion was inhibited by previous administration of MWE. It is conclude that MWE elicits hypotensive action in the rabbit by the centrally induced cholinergic effect and the inhibitation of responses to sypathetic adrenergic nerve activation.

• YAKHAK HOEJI
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• v.17 no.2
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• pp.103-110
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• 1973

In this study the effect of alcohol extract of atractlis (AAE) on the blood pressure of the rabbit was investigated. The results of the experiment are as follows. AAE elicited hypotension with doses ranging from 3 to 30 mg/kg, i.v., exhibiting a linear dose-relationship. This effect of AAE was abolished by atropine and potentiated by physostigmine, while not affected by diphenhydramine, hexamethonium, propranolol and cyproheptadine. AAE did not influence the pressor responses to norepinephrine and the depressor to isoproterenol. The above results indicate that AAE produced the hypotension by stimulating the parasympathetic nervous system related to acetylcholine.

• The Korean Journal of Pharmacology
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• v.27 no.1
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• pp.21-31
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• 1991

When administered intracerebroventricularly (icv), cholinergic nicotinic agents, nicotine and DMPP, as well as cholinergic muscarinic agents, muscarine and bethanechol, produced pressor responses in urethane-anesthetized vagotomized rabbits. The response patterns to nicotine and to DMPP were similar, while the bethanechol response resembled the muscarine pattern. The pressor response to nicotine and DMPP was markedly inhibited by icv mecamylamine but not by icv pirenzepine, whereas the response to muscarine and bethanechol was inhibited by icv pirenzepine but not by icv mecamylamine, suggesting that both nicotinic and muscarinic receptors in the brain are involved in the action. Intravenous pretreatments of animals with regitine, reserpine, enalapril, saralasin, both regitine and enalapril, both regitine and saralasin, SK&F-100273 did not prevent the pressor response to nicotine and muscarine. Iv pretreatments with both regitine and SK&F-100273 inhibited the nicotine response without affecting the muscarine response, whereas pretreatments with three agents, regitine, enalapril and SK&F-100273, inhibited the muscarine response. The nicotine-induced elevated blood pressure as well as the muscarine-induced were lowered by regitine but not by enalapril or by SK&F-100273. Enalapril was without effect on the nicotine hypertension in rabbits treated with regitine or both regitine and SK&F-100273, whereas SK&F-100273 lowered the nicotine hypertension in regitine-treated animals. Enalapril did not enhance the lowering effect of SK&F-100273 in regitine-treated ones, nor did it cause a fall of the muscarine hypertension induced in regitine-treated rabbits, but it did lower the blood pressure in animals treated with both regitine and SK&F-100273. Likewise, SK&F-100273 did not cause a fall of the muscarine hypertension induced in regitine-treated rabbits, but it did lower the blood pressure in animals treated with both regitine and enalapril. These data suggest that the nicotine-induced hypertensive state is related to at least two systems in the periphery-sympathetic and vasopressin, whereas in the muscarine-induced hypertensive state three systems in the periphery are involved, i.e., the sympathetic, vasopressin and angiotensin system. The hypotensive effect of regitine on basal arterial blood pressure levels of rabbits was not influenced by pretreatment with either of enalapril or SK&F-100273, but significantly potentiated by treating with both enalapril and SK&F-100273, suggesting participation of the sympathetic and the renin-angiotensin system as well as the vasopressin system in maintenance of arterial blood pressure.

• The Korean Journal of Physiology
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• v.16 no.2
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• pp.129-136
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• 1982

We studied this experiment to compare the effects of exercise and other body conditions: i.e., Flack test, cold pressor test and bicycle ergometry on the electrocardiogram. We had sixty healthy college students who were thirty nine men and twenty one women. Their $mean{\pm}SD$ values of physical characteristics were as follows: age; $22.0{\pm}1.4$, weight; men $61.7{\pm}5.6\;kg$, women $46.2{\pm}7.47\;kg$. We observed the changes of P-Q and Q-T interval, R and T amplitude, mean QRS vector, S-T segment deviation, and P and T vector. The result obtained were summarized as follows: P vector was shifted rightward regardless of the type of stress. T vector was shifted var-in each stress but in the bicycle ergometry T vector was shifted leftward. Mean QRS vector was shifted rightward immediately after the bicycle ergometry. Percentage of the occurrence of the depression of S-T segment was 21.7% at the immediately after the submaximal bicycle ergometry in lead II. The elevation of S-T segment was often observed after the mild stresses. Increased amplitude of T wave in the cold pressor test and decreased amplitude of T wave in the bicycle ergometry were observed. In the bicycle ergometry and other stresses, the precise mechanism of S-T segment changes was unexplained but insufficient repolarization in base or apex of the left ventricle due to heart strain was indicated by so called S-T vector analysis.

• YAKHAK HOEJI
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• v.37 no.6
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• pp.605-614
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• 1993

To investigate the endothelial dependence of angiotensin II(A II)-induced responses in the systemic and pulmonary arterial system of acute renal hypertensive rats of 2-kidney, 1-ligation type (RHRs), A II-induced vasocontractile and pressor effects were evaluated in isolated arteries and in vivo, respectively. A II dose-dependently contracted intact thoracic aorta and pulmonary artery (E$_{max}$:40% at 10$^{-7}$M and 80% at 3$\times$10 $^{-8}$M, respectively) from normotensive rats(NRs), which was significantly increased by removal of endothelial cells or pretreatment with EDRF inhibitors. In NRs, A II increased mean systemic and pulmonary arterial pressure(33 and 5.6mmHg at 0.1 $\mu\textrm{g}$/kg, respectively), the effect being significantly increased (P<0.01) by L-NAME(30mg/kg, i.v.). However, A II-induced contraction of intact thoracic aorta and pulmonary artery(E$_{max}$: 33% at 10$^{-7}$M and 93% at 3$\times$10$^{-8}$M, respectively) from RHRs were not changed after endothelial function was disrupted as above; similarly, pressor effects of A II on the systemic and pulmonary arterial pressure in RHRs did not altered by L-NAME. A II tachyphylactic responses for intact thoracic aorta from NRs and RHRs(65 and 87% at 10$^{-8}$M, respectively) were greater than those for pulmonary artery(19 and 19% at 10$^{-8}$M, respectively). Distruption of endothelial function significantly (P<0.01) depressed A II tachyphylaxis for thoracic aorta, but not for pulmonary artery. These results suggest that vascular reactivity to A II is not altered in RHRs, and it is greater for pulmonary arterial system than for systemic arterial system. A II reactivity is EDRF-dependent in both arterial systems of NRs, but EDRF-independent for RHRs. Finally, EDRF is one of the major factors underlying A II tachyphylaxis for thoracic aorta, but not for pulmonary artery.

• Journal of Pharmaceutical Investigation
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• v.8 no.1
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• pp.6-16
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• 1978

We obtained 4 kinds of extract fraction from Acanthopanacis Radicis Cortex and studied on the influence to the blood pressure of rabbit. These 4 fractions were obtained as follows; Fraction I was insoluble fraction by 99% ethanol from 80% methanol extract of Acanthopanacis Radicis Cortex, fraction II, precipitated fraction by ether from 99% ethanol soluble fraction of 80% methanol extract of Acanthopanaacis Radicis Cortex, fraction III, no precipitated fraction by ether from 99% ethanol soluble fraction of above 80% methanol extract and fraction IV, water extract of Acanthopanacis Radicis Cortex. All of fractions, when administered into ear-vein of rabbit, produced fall of blood pressure. Among these 4 fractions, although fraction III was not only the most potent but had the greatest efficacy, we observed the mechanism of hypotensive action of Acanthopanacis Radicis Cortex, making use of fraction II which was thought as a comparatively pure fraction. Hypotensive action of fraction II (APF II) was not affected by vagotominization but markedly inhibited by atropine. Pretreatment of bethanidine showed a tendency to weaken the depressor action of APF II, although it was not a significant result, but diphenhydramine did not influence APF II action. Phentolamine, guanethidine and chlorisondamine inhibited significantly the hypotensive action of APF II. APF II elicited the potentiation of norepinphrine pressor action dependent on the time-factor whereas it did not influence angiotesin pressor action. It is seemed that APF II exhibited hypotensive action, causing peripheral muscarinic-effect and centrally induced sympatholytic action.

• The Korean Journal of Pharmacology
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• v.14 no.1_2
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• pp.13-23
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• 1978

1) It was attempted to clarify the sites of action of central (either intraventricular or intracisternal) norepinephrine(NE) and clonidine to cause cardiac slowing and hypotension in urethane-anesthetized rabbits. 2) NE produced cardiac slowing but indistinct effect on blood pressure. Clonidine produced cardiac slowing and hypotension. 3) Intraventricular and intracisternal administration of NE, clonidine, phenylephrine and isoproterenol did not make difference in their effects, except that the onset of cardiac slowing by intracisternal NE was more rapid than intraventricular NE. 4) Upon repeated administration of NE at the intervals of about two hours, blood pressure responses changed to the pressor ones, the cardiac slowing unchanged. By this procedure the cardiac slowing as well as the hypotension by clonidine were gradually diminished. 5) Clonidine, when given during the NE effects were persisting, did not produce the lowering of blood pressure and further decrease of heart rate. NE, when given during the clonidine effects were persisting, produced marked elevation of blood pressure but did not produce further decrease of heart rate. 6) After intraventricular administration of regitine or desmethylimipramine, the cardiac slowing effect of NE and the clonidine effects were not observed, whereas NE produced marked elevation of blood pressure. 7) Reserpinized rabbits showed pressor and cardiac accelerating responses to NE; slight pressor, and little cardiac responses to clonidine. 8) It seems that the cardiac slowing by both clonidine and NE as well as the hypotetsion by clonidine are mediated by the presynaptic ${\alpha}$-adrenoceptor in the brain but the pressor responses to NE and clonidine are mediated by other site(s) than the presynaptic ones.

• Journal of Life Science
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• v.20 no.7
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• pp.969-976
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• 2010

In vivo studies of KR-31125 (2-butyl-5-dimethoxymethyl-6-phenyl-7-methyl-3-[[2'-(1H-tetrazol-5-yl) biphenyl-4-yl]methyl]-3H-imidazo[4,5-b]pyridine) were performed in pithed rats, conscious angiotensin II (AII) challenged normotensive rats, renal hypertensive rats (RHRs) and furosemide-treated beagle dogs. KR-31125 induced a non-parallel right shift in the dose-pressor response curve to AII ($ID_{50}$: 0.095 mg/kg) with a dose-dependent reduction in the maximum responses in pithed rats. Compared to losartan, this antagonistic effect was about 18 times more potent, presenting competitive antagonism. Other agonists such as norepinephrine and vasopressin did not alter the responses induced by KR-31125. Orally administered KR-31125 had no agonistic effect and dose-dependently inhibited the pressor response to AII with a slightly weaker potency ($ID_{50}$: 0.25 and 0.47 mg/kg, respectively) in the AII-challenged normotensive rat model, but with a more rapid onset of action than losartan (time to $E_{max}$: 30 min for KR-31125 and 6 hr for losartan). KR-31125 produced a dose-dependent antihypertensive effect with a higher potency than losartan in RHRs, and these effects were confirmed in furosemide-treated dogs where they presented a dose-dependent and long-lasting (>8 hr) antihypertensive effect with a rapid onset of action (time to $E_{max}$: 2-4 hr), as well as a 20-fold greater potency than losartan. These results suggest that KR-31125 is a potent, orally active $AT_1$ receptor antagonist that can be applied to the development of new diagnostic and research tools as an added exploratory potential of $AT_1$ receptor antagonist.

• The Korean Journal of Pharmacology
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• v.22 no.2
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• pp.115-122
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• 1986

To delineate the relationship between subtypes of central alpha-adrenoceptor and central calcium channel, influences of intracerebroventricular (icv) diltiazem and nifedipine on the changes of blood pressure and heart rate by icv methoxamine and clonidine were investigated in urethane-anesthetized rabbits. 1) Methoxamine (1mg, icv) produced pressor and bradycardiac effect and clonidine $(30\;{\mu}g,\;icv)$ produced hypotension and bradycardia. 2) Icv diltiazem and nifedipine elicited dose-dependent deprcssor and bradycardiac responses. The depressor response to nifedipine was more prominent than that to diltiazem but the bradycardiac effect of nifedipine was smaller than that of diltiazem. The depressor responses to icy nifedipine $(35{\mu}g)$ and icv diltiazem $(400{\mu}g)$ were persistent but those to intravenous (iv) nifedipine $(35{\mu}g/kg)$ and diltiazem $(200{\mu}g/kg)$ were transient. 3) The pressor response to methoxamine was little affected by pretreatment with in diltiazem $(400{\mu}g)$ or icv nifedipine $(35,\;350{\mu}g)$ but the bradycardiac response to methoxamine was significantly attenuated by the same pretreatment. 4) The depressor response to clonidine was markedly attenuated by pretreatment with icv diltiazem $(400{\mu}g)$ or icv nifedipine $(35,\;350{\mu}g)$ but not affected by pretreatment with iv diltiazem $(200{\mu}g/kg)$ or iv nifedipine $(20{\mu}g/kg)$. Pretreatment with icv and iv diltiazem or nifedipine reduced the bradycardiac effect of clonidine. 5) Pretreatment with icv clonidine had no effect on the depressor and bradycardiac responses to in diltiazcm or icv nifedipine. These results indicate that diltiazem and nifedipine have no effect on icv methoxamine-induced pressor response elicited by the activation of central alpha-l adrenoceptors whereas the icv clonidine-induccd depressor and bradycardiac effects which result from the activation of central alpha-2 adrenoceptors are inhibited by the calcium antagonists.