• Proceedings of the Korean Society of Applied Pharmacology
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• 2005.11a
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• pp.5-9
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• 2005

• 대한임상약리학회:학술대회논문집
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• 1996.12a
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• pp.46-46
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• 1996

• Proceedings of the PSK Conference
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• 2001.04a
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• pp.217.1-217.1
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• 2001

• Proceedings of the PSK Conference
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• 2001.04a
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• pp.220.2-220.2
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• 2001

• The Korean Journal of Physiology and Pharmacology
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• v.2 no.1
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• pp.55-62
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• 1998

${\alpha},\;{\beta}-Adrenergics$, and calcium channels were known to be related to inducing cardiac hypertrophy. Recently, it was reported that the cardiac renin-angiotensin system (RAS) was an important factor in ventricular hypertrophy. The present study was aimed to investigate the effects of ${\alpha},\;{\beta}-adrenergic$, and calcium channel blockers that might be involved in the regulation of cardiac RAS. The reverse transcription-polymerase chain reaction (RT-PCR) was used to detect the expression of renin gene in the perfused rat heart. Changes in angiotensin converting enzyme (ACE) activity and cyclic AMP (cAMP) content which were thought to play a role in inducing cardiac hypertrophy were measured in the perfused rat heart. The expression of renin gene was not only increased by isoproterenol with metoprolol-pretreatment but also increased by vasopressin treatment in the presence of calcium channel blocker, nifedipine or verapamil. Either prazosin alone or norepinephrine with prazosin-pretreatment significantly increased the ACE activity. However, isoproterenol with metoprolol-pretreatment significantly decreased the ACE activity. On the other hand, the ACE activity was not changed by vasopressin, nifedipine, or verapamil treatments. The content of cAMP was significantly increased by either isoproterenol or vasopressin treatment. According to these results, renin gene expression was associated with ${\beta}2$ - adrenoceptor and calcium channel. ACE activity was associated with ${\alpha}-\;and{\beta}2$ - adrenoceptor. In conclusion, ${\beta}2$ - adrenoceptor was important in cardiac renin gene expression and ACE activity and ${\alpha},\;{\beta}$ -adrenergic, and calcium channel blockers might be involved in the regulation of cardiac RAS in a complicated way.

• Proceedings of the Korean Society of Applied Pharmacology
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• 1993.04a
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• pp.93-93
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• 1993

도파민 D 수용체 및 5-HT 수용체 차단기전을 지닌 새로운 항정신분열증 약물인 risperidone은 활성형 대사물로 9-OH risperidone을 체내에서 생성하는 바, 이 대사과정의 유전적 다형성의 여부 즉 hydroxylation 과정에 CYPIID6의 관여 여부를 검토코자 하였다. Metoprolol 100 mg 경구투여로 CYPIID6의 대사능의 표현형을 결정한 12명의 정상 피험자(11명: extensive metabolizer, 1명: poor metabolizer)를 대상으로 하였으며, 피험자는 risperidone 1 또는 2 mg 경구투여후 혈중 risperidone 및 9-OH risperidone 농도를 경시적으로 radioimmunoassay법으로 측정하였다. 이들 피험자중 6명의 extensive metabolizer는 quinidine 600 mg/day의 용량 투여로 CYPIID6의 활성도를 완전 억제시킨 후 risperidone 1 mg 경구투여에 따른 약동학적 성상을 재검토하여 risperidone hydroxylation에 CYPIID6의 관여 여부를 검토하였다. 1) 1명의 poor metabolizer는 extensive metabolizer에 비해 현저히 긴 risperidone 반감기를 보였다. 2) 12명의 피험자에서 관찰된 metoprolol metabolic ratio는 risperidone 혈장 반감기 및 log(risperidone AUC/9-OH-risperidone AUC)와 유의한 상관성을 나타내었다. 3) Quinidine 투여는 risperidone의 반감기의 유의한 증가와 9OH risperidone AUC의 현저한 감소를 보였으나, 9-hydroxylation 대사과정이 완전히 억제되지는 않았다.

• 대한임상약리학회:학술대회논문집
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• 1996.12a
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• pp.36-36
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• 1996

• Proceedings of the PSK Conference
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• 2003.10b
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• pp.219.3-219.3
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• 2003

We describe here solid-extraction and derivatisation methods of ${\beta}$-adrenoceptor blocking drugs used for the treatment of various cardiovascular disorders such as hypertension, angina pectoris and cardiac arrhythmia: propranolol, metoprolol, sotalol, timolol, oxprenolol, alpranolol, atenolol, pindolol. Solid-extraction and derivatisation methods are described involving the use of Bond Elut Certify cartridges, MSTFA and MBTFA. Gas chromatographic-mass spectrometry analysis(GC/MS) was carried out select-ion monitroing mode. (omitted)

• Journal of Environmental Analysis, Health and Toxicology
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• v.21 no.4
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• pp.243-251
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• 2018

Pharmaceuticals in wastewater effluents have been recognized as emerging pollutants threatening freshwater organisms. To extend understanding for bioaccumulation and toxicity in those organisms, information on biotransformation products (or metabolites) and their metabolic pathway are crucial. The aim of the present study is to identify and elucidate metabolites of pharmaceuticals formed in exposed organisms using suspect and nontarget screening approach using LC-HRMS. As the target pharmaceuticals, carbamazepine, ketoprofen, metoprolol, propranolol, and verapamil were selected whereas Daphnia magna and Gammarus pulex were used as test organisms. After 24h exposure, metabolites formed in the organisms were identified using LC-HRMS. The structures of metabolites were elucidated via analysis of MS/MS fragment pattern and the comparison with fragment database. As the results, a total of 10 metabolites were identified for 5 parent compounds (C253/C356 for carbamazepine, K211 for ketoprofen, M256 for metoprolol, P218/P276/P306 for propranolol, V196/V291/V441 for verapamil). Among them, the presence of C253 and V291 was confirmed using standard materials. Most of the identified metabolites were formed through oxidative reactions such as hydroxylation, N-demethylation, and dealkylation. Cysteine conjugation (phase II reaction) metabolite (C356) for carbamazepine was found in daphnia. The metabolic pathway of verapamil showed similar metabolic pathways and metabolic pathways for both species. Although the toxicological information on the identified metabolites could not be confirmed, the molecular structure information of the proposed metabolites can be used for future evaluation and prediction of toxicity.

• Journal of Pharmaceutical Investigation
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• v.29 no.2
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• pp.117-126
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• 1999

Differential scanning calorimetry(DSC) was used as a screening technique for assessing the compatibility of some drugs with excipients. On the basis of DSC results, interaction of ibuprofen with PVP K40 was found and eutectic formations with PEG 6000 or magnesium stearate were demonstrated. Fenoprofen Ca was found to interact with PEG 6000. Naproxen showed interactions with PEG 6000, PVP K40, PVPP and Mg stearate. Interactions of tiaprofenic acid with PVP K40 or PVPP were found and eutectic formations with PEG 6000 or Mg stearate were observed. Bisoprolol hemifumarate, metoprolol tartrate and penbutolol sulfate were found to interact with lactose.