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6) ³»Àμº ÇÁ·Î½ºÅ¸±Û¶õµò ÇÕ¼ºÀúÇØÁ¦ : Àεµ¸ÞŸ½ÅÀº ƯÈ÷ ·¹´Ñ ³óµµ°¡ ³·Àº °íÇ÷¾ÐÀÇ °æ¿ì İÅäÇÁ¸±ÀÇ Ç÷¾Ð°ÇÏÀÛ¿ëÀ» °¨¼Ò½Ãų ¼ö ÀÖ´Â °ÍÀ¸·Î º¸°íµÈ ¹Ù ÀÖ´Ù. ±âŸ ºñ½ºÅ×·ÎÀ̵强 ¼Ò¿°Á¦µµ ÀÌ¿Í °°Àº ÀÛ¿ëÀ» ÇÒ ¼ö ÀÖ´Ù.
7) Ŭ·Î´Ïµò : İÅäÇÁ¸±ÀÇ Ç÷¾Ð°ÇÏÀÛ¿ëÀÌ Å¬·Î´ÏµòÀ» Åõ¿©ÇÏ´ø ȯÀÚ¿¡°Ô ÀÌ ¾àÀ» ¹Ù²Ù¾î Åõ¿©ÇÒ °æ¿ì Áö¿¬µÉ ¼ö ÀÖ´Ù.
8) ¾Ë·ÎǪ¸®³î, ÇÁ·ÎÄ«Àξƹ̵å : İÅäÇÁ¸±°ú ¾Ë·ÎǪ¸®³î ¶Ç´Â ÇÁ·ÎÄ«Àξƹ̵带 º´¿ëÅõ¿©½Ã È£Áß±¸°¨¼Ò³ª ÇǺÎÁ¡¸·¾ÈÁõÈıº(Stevens-Johnson ÁõÈıº)ÀÌ ³ªÅ¸³µ´Ù´Â º¸°í°¡ ÀÖ´Ù. ºñ·Ï Àΰú°ü°è´Â È®¸³µÇÁö ¾Ê¾ÒÀ¸³ª ÀÌ·¯ÇÑ º´¿ëÅõ¿©´Â ÁÖÀÇÇÑ´Ù(ƯÈ÷ ½ÅÀå¾Ö ȯÀÚ).
9) ¸é¿ª¾ïÁ¦Á¦ : ¾ÆÀÚÆ¼¿ÀÇÁ¸°, ½ÃŬ·ÎÆ÷½ºÆÄ¹Ìµå¿Í İÅäÇÁ¸±À» Åõ¿©¹Þ°í ÀÖ´Â ½ÅÀå¾Ö ȯÀÚ¿¡¼ Ç÷¾×Áúȯ°ú °ü·ÃÀÖ´Ù´Â º¸°í°¡ ÀÖ´Ù.
10) ÇÁ·Îº£³×½Ãµå : İÅäÇÁ¸±ÀÇ ½Åû¼ÒÀ²Àº ÇÁ·Îº£³×½Ãµå¿¡ ÀÇÇØ °¨¼ÒµÈ´Ù.
11) ACEÀúÇØÁ¦¿Í ¸®Æ¬ÀÇ º´¿ëÅõ¿©½Ã Ç÷û ¸®Æ¬³óµµÀÇ »ó½Â°ú ¸®Æ¬µ¶¼º Áõ»óÀÌ º¸°íµÇ¾î ÀÖÀ¸¹Ç·Î Ç÷û ¸®Æ¬³óµµ¸¦ ÀÚÁÖ ¸ð´ÏÅÍÇÏ¸ç ½ÅÁßÈ÷ Åõ¿©ÇÑ´Ù.
12) ¾ÈÁö¿ÀÅٽмö¿ëü Â÷´ÜÁ¦(ARB), ¾ÈÁö¿ÀÅٽŠÀüȯ È¿¼Ò(ACE) ¾ïÁ¦Á¦ ¶Ç´Â ·¹´Ñ¾ïÁ¦Á¦(¾Ë¸®½ºÅ°·»)ÀÇ º´¿ëÅõ¿©¿¡ ÀÇÇÑ ·¹´Ñ-¾ÈÁö¿ÀÅٽŰè(RAS)ÀÇ ÀÌÁßÂ÷´ÜÀº ÀúÇ÷¾Ð, ½Ç½Å, °íÄ®·ýÇ÷Áõ ¹× ½Å±â´ÉÀÇ ÀúÇÏ(±Þ¼º½ÅºÎÀüÁõ Æ÷ÇÔ)¿Í °°Àº ÀÌ»ó»ç·ÊÀÇ ºóµµ°¡ ·¹´Ñ-¾ÈÁö¿ÀÅٽŰè(RAS)¿¡ ¿µÇâÀ» ¹ÌÄ¡´Â ¾àÁ¦ÀÇ ´Üµ¶ »ç¿ë½Ã¿¡ ºñÇØ ³ô´Ù. ÀÌ ¾à°ú ·¹´Ñ¾ïÁ¦Á¦(¾Ë¸®½ºÅ°·») ÇÔÀ¯ Á¦Á¦ÀÇ º´¿ëÀº ±ÇÀåµÇÁö ¾ÊÀ¸¸ç, ´ç´¢º´À̳ª Áߵ¡ÁßÁõÀÇ ½ÅÀå¾Ö ȯÀÚ(GFR <60 ml/min/1.73§³ )´Â º´¿ëÅõ¿©Çؼ´Â ¾ÈµÈ´Ù. ÀÌ ¾à°ú ¾ÈÁö¿ÀÅٽмö¿ëü Â÷´ÜÁ¦(ARB)ÀÇ º´¿ëÀº ±ÇÀåµÇÁö ¾ÊÀ¸¸ç, ´ç´¢º´¼º ½ÅÁõ ȯÀÚ´Â º´¿ëÅõ¿©Çؼ´Â ¾ÈµÈ´Ù.
13) mTOR(mammalian target of rapamycin) ÀúÇØÁ¦¿Í º´¿ëÅõ¿©ÇÏ´Â °æ¿ì¿¡´Â Ç÷°üºÎÁ¾ À§ÇèÀÌ Áõ°¡ÇÒ ¼ö ÀÖÀ¸¹Ç·Î ÁÖÀÇÇÑ´Ù.
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11) Ä®½·¿° : ¹è¼³°¨¼Ò·Î ÀÎÇØ Ç÷Áß Ä®½·³óµµ°¡ »ó½ÂµÉ ¼ö ÀÖ´Ù.
12) °½É¹è´çü : ÀúÄ®·ýÇ÷Áõ°ú °ü·ÃµÈ µð±âÅ»¸®½ºµ¶¼ºÀÌ Áõ°¡ÇÒ ¼ö ÀÖÀ¸¹Ç·Î Ä®½·³óµµ¸¦ ¸ð´ÏÅÍÇÑ´Ù.
13) ÄÝ·¹½ºÆ¼¶ó¹Î, ÄÝ·¹½ºÆ¼Æú : Ä¡¾ÆÁþ°è ÀÌ´¢Á¦ÀÇ Èí¼ö¸¦ Áö¿¬ ¶Ç´Â °¨¼Ò½Ãų ¼ö ÀÖ´Ù. Ä¡¾ÆÁþ°è ÀÌ´¢Á¦´Â ÀÌ·¯ÇÑ ¾à¹°À» Åõ¿©Çϱâ 1½Ã°£ ÀüÀ̳ª 4-6½Ã°£ ÈÄ¿¡ Åõ¿©ÇÑ´Ù.
14) µð¾ÆÁ·½Ãµå : °íÇ÷´ç, °í´¢»êÇ÷Áõ, Ç÷¾Ð°ÇÏÀÛ¿ëÀÌ Áõ°µÉ ¼ö ÀÖÀ¸¹Ç·Î. Ç÷´ç°ú ¿ä»êÄ¡¸¦ ¸ð´ÏÅÍÇÑ´Ù.
15) MAOÀúÇØÁ¦ : Ç÷¾Ð°ÇÏÀÛ¿ëÀÌ Áõ°µÇ¹Ç·Î ¿ë·®Á¶ÀýÀÌ ÇÊ¿äÇÏ´Ù.
16) ºñ½ºÅ×·ÎÀ̵强 ¼Ò¿°Á¦ : ÀÌ´¢Á¦ÀÇ È¿°ú¸¦ °¨¼Ò½Ãų ¼ö ÀÖ´Ù.
17) ¸ÞÅ׳ª¹Î : ¿ä¸¦ ¾ËÄ®¸®ÈÇÏ¿© È¿°ú¸¦ °¨¼Ò½Ãų ¼ö ÀÖ´Ù.
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| º¸°ü»ó ÁÖÀÇ |
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| Á¶Á¦½Ã ÁÖÀÇ |
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 | ÇмúÁ¤º¸ |
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| Ç׸ñ |
³»¿ë |
| DUR (ÀǾàǰ»ç¿ëÆò°¡) |
º´¿ë±Ý±â :
°í½ÃµÈ º´¿ë±Ý±â ³»¿ëÀº ¾ø½À´Ï´Ù.
[»óÈ£ÀÛ¿ë/º´¿ë±Ý±â°Ë»ö]
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°í½ÃµÈ ¿¬·É±Ý±â ³»¿ëÀº ¾ø½À´Ï´Ù.
[¿¬·É´ë±Ý±â»ó¼¼°Ë»ö]
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| µ¶¼ºÁ¤º¸ |
Captopril¿¡ ´ëÇÑ µ¶¼ºÁ¤º¸ : Á¤º¸º¸±â
Ãâó: ±¹¸³µ¶¼º°úÇпø µ¶¼º¹°ÁúÁ¤º¸DB : http://www.nitr.go.kr/nitr/contents/m134200/view.do |
| Mechanism of Action |
Captopril¿¡ ´ëÇÑ Mechanism_Of_Action Á¤º¸ Captopril competes with angiotensin I for binding at the angiotensin-converting enzyme, blocking the conversion of angiotensin I to angiotensin II. As angiotensin II is a vasoconstrictor and a negative feedback mediator for renin activity, lower angiotensin II levels results in a decrease in blood pressure, an increase in renin activity, and stimulation of baroreceptor reflex mechanisms. Kininase II, an enzyme which degrades the vasodilator bradykinin, is identical to ACE and may also be inhibited.
Hydrochlorothiazide¿¡ ´ëÇÑ Mechanism_Of_Action Á¤º¸ As a diuretic, hydrochlorothiazide inhibits active chloride reabsorption at the early distal tubule via the Na-Cl cotransporter, resulting in an increase in the excretion of sodium, chloride, and water. Thiazides like hydrochlorothiazide also inhibit sodium ion transport across the renal tubular epithelium through binding to the thiazide sensitive sodium-chloride transporter. This results in an increase in potassium excretion via the sodium-potassium exchange mechanism. The antihypertensive mechanism of hydrochlorothiazide is less well understood although it may be mediated through its action on carbonic anhydrases in the smooth muscle or through its action on the large-conductance calcium-activated potassium (KCa) channel, also found in the smooth muscle.
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| Pharmacology |
Captopril¿¡ ´ëÇÑ Pharmacology Á¤º¸ Captopril, an angiotensin-converting enzyme (ACE) inhibitor, is used to treat hypertension, congestive heart failure, and renal syndromes such as diabetic nephropathy and scleroderma. The adverse effect and pharmacokinetic limitations of captopril stimulated the development enalapril and subsequent ACE inhibitors.
Hydrochlorothiazide¿¡ ´ëÇÑ Pharmacology Á¤º¸ Thiazides such as hydrochlorothiazide promote water loss from the body (diuretics). They inhibit Na+/Cl- reabsorption from the distal convoluted tubules in the kidneys. Thiazides also cause loss of potassium and an increase in serum uric acid. Thiazides are often used to treat hypertension, but their hypotensive effects are not necessarily due to their diuretic activity. Thiazides have been shown to prevent hypertension-related morbidity and mortality although the mechanism is not fully understood. Thiazides cause vasodilation by activating calcium-activated potassium channels (large conductance) in vascular smooth muscles and inhibiting various carbonic anhydrases in vascular tissue.
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| Metabolism |
Captopril¿¡ ´ëÇÑ Metabolism Á¤º¸ # Phase_1_Metabolizing_Enzyme:Cytochrome P450 2D6 (CYP2D6)
Hydrochlorothiazide¿¡ ´ëÇÑ Metabolism Á¤º¸ # Phase_1_Metabolizing_Enzyme:Not Available
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| Protein Binding |
Captopril¿¡ ´ëÇÑ ´Ü¹é°áÇÕ Á¤º¸ About 25-30% of the circulating drug is bound to plasma proteins
Hydrochlorothiazide¿¡ ´ëÇÑ ´Ü¹é°áÇÕ Á¤º¸ 67.9%
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| Half-life |
Captopril¿¡ ´ëÇÑ ¹Ý°¨±â Á¤º¸ Less than 3 hours
Hydrochlorothiazide¿¡ ´ëÇÑ ¹Ý°¨±â Á¤º¸ 5.6 and 14.8 hours
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| Absorption |
Captopril¿¡ ´ëÇÑ Absorption Á¤º¸ 75% without food (the presence of food in the gastrointestinal tract reduces absorption by about 30 to 40 percent).
Hydrochlorothiazide¿¡ ´ëÇÑ Absorption Á¤º¸ 50-60%
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| Pharmacokinetics |
CaptoprilÀÇ ¾à¹°µ¿·ÂÇÐÀÚ·á
- Ç÷¾Ð°ÇÏ ÃÖ´ëÈ¿°ú ¹ßÇö½Ã°£ : 1-1.5 ½Ã°£
- ÀÛ¿ëÁö¼Ó½Ã°£ : ¿ë·®ÀÇÁ¸Àû. Àå±â°£ Ä¡·á½Ã Ç÷¾Ð°ÇÏ ÃÖ´ëÈ¿°ú°¡ ³ªÅ¸³ª´Â µ¥¿¡´Â ¼ö ÁÖ°¡ ÇÊ¿äÇÒ ¼ö ÀÖ´Ù.
- ÃÖ°íÇ÷Áß³óµµ µµ´Þ½Ã°£ : 1-2 ½Ã°£ À̳»
- Èí¼ö : 60-75%
- ´Ü¹é°áÇÕ : 25-30%
- ´ë»ç : 50%
- ¹Ý°¨±â : ½Å±â´É°ú ½É ±â´É¿¡ µû¶ó Á¿ìµÈ´Ù.
- Á¤»ó ¼ºÀÎ : 1.9 ½Ã°£
- ¿ïÇ÷¼º½ÉºÎÀü ȯÀÚ : 2.06 ½Ã°£
- ¹«´¢Áõ : 20-40 ½Ã°£
- ¼Ò½Ç : 24½Ã°£ ³»¿¡ 95%°¡ ¼Òº¯À¸·Î ¹è¼³µÈ´Ù.
HydrochlorothiazideÀÇ ¾à¹°µ¿·ÂÇÐÀÚ·á
- ÀÌ´¢È¿°ú ¹ßÇö½Ã°£ : °æ±¸ : 2½Ã°£ À̳»
- ÃÖ´ëÈ¿°ú ¹ßÇö½Ã°£ : 4½Ã°£
- ÀÛ¿ëÁö¼Ó½Ã°£ : 6-12½Ã°£
- Èí¼ö : °æ±¸ : 60-80%
- ¼Ò½Ç : ¹Ìº¯Èü·Î ½Å¹è¼³µÈ´Ù.
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| Biotransformation |
Captopril¿¡ ´ëÇÑ Biotransformation Á¤º¸ Hepatic
Hydrochlorothiazide¿¡ ´ëÇÑ Biotransformation Á¤º¸ Hydrochlorothiazide is not metabolized.
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| Toxicity |
Captopril¿¡ ´ëÇÑ Toxicity Á¤º¸ Symptoms of overdose include coma, lethargy, low blood pressure, sluggishness, and stomach and intestinal irritation and hyperactivity.
Hydrochlorothiazide¿¡ ´ëÇÑ Toxicity Á¤º¸ The most common signs and symptoms observed are those caused by electrolyte depletion (hypokalemia, hypochloremia, hyponatremia) and dehydration resulting from excessive diuresis. If digitalis has also been administered, hypokalemia may accentuate cardiac arrhythmias. The oral LD50 of hydrochlorothiazide is greater than 10 g/kg in the mouse and rat.
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| Drug Interactions |
Captopril¿¡ ´ëÇÑ Drug_Interactions Á¤º¸ Amiloride Increased risk of hyperkaliemiaDrospirenone Increased risk of hyperkaliemiaLithium The ACE inhibitor increases serum levels of lithiumPotassium Increased risk of hyperkaliemiaSpironolactone Increased risk of hyperkaliemiaTizanidine Tizanidine increases the risk of hypotension with the ACE inhibitorTriamterene Increased risk of hyperkaliemia
Hydrochlorothiazide¿¡ ´ëÇÑ Drug_Interactions Á¤º¸ Amantadine The diuretic increases the adverse effect of amantadineDeslanoside Possible electrolyte variations and arrhythmiasDigitoxin Possible electrolyte variations and arrhythmiasDigoxin Possible electrolyte variations and arrhythmiasLithium The thiazide diuretic increases serum levels of lithiumDofetilide Increased risk of cardiotoxicity and arrhythmiasDiazoxide Significant hyperglycemic effect
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CYP450 Drug Interaction |
[CYP450 TableÁ÷Á¢Á¶È¸]
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| Food Interaction |
Captopril¿¡ ´ëÇÑ Food Interaction Á¤º¸ Avoid alcohol.Avoid salt substitutes containing potassium.Take on empty stomach: 1 hour before or 2 hours after meals, food decreases absorption by 30 to 55%.Avoid natural licorice.Do not take calcium, aluminum, magnesium or Iron supplements within 2 hours of taking this medication.
Hydrochlorothiazide¿¡ ´ëÇÑ Food Interaction Á¤º¸ Avoid alcohol.Avoid excess salt/sodium unless otherwise instructed by your physician.Take with food.Increase potassium intake; add a banana or orange juice; unless instructed otherwise.Avoid natural licorice.Do not take calcium, aluminum, magnesium or Iron supplements within 2 hours of taking this medication.
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| Drug Target |
[Drug Target]
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| Description |
Captopril¿¡ ´ëÇÑ Description Á¤º¸ A potent and specific inhibitor of peptidyl-dipeptidase A. It blocks the conversion of angiotensin I to angiotensin II, a vasoconstrictor and important regulator of arterial blood pressure. Captopril acts to suppress the renin-angiotensin system and inhibits pressure responses to exogenous angiotensin. [PubChem]
Hydrochlorothiazide¿¡ ´ëÇÑ Description Á¤º¸ A thiazide diuretic often considered the prototypical member of this class. It reduces the reabsorption of electrolytes from the renal tubules. This results in increased excretion of water and electrolytes, including sodium, potassium, chloride, and magnesium. It has been used in the treatment of several disorders including edema, hypertension, diabetes insipidus, and hypoparathyroidism. [PubChem]
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| Dosage Form |
Captopril¿¡ ´ëÇÑ Dosage_Form Á¤º¸ Tablet Oral
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| Drug Category |
Captopril¿¡ ´ëÇÑ Drug_Category Á¤º¸ Angiotensin-converting Enzyme InhibitorsAntihypertensive Agents
Hydrochlorothiazide¿¡ ´ëÇÑ Drug_Category Á¤º¸ Antihypertensive AgentsDiureticsSodium Chloride Symporter Inhibitors
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| Smiles String Canonical |
Captopril¿¡ ´ëÇÑ Smiles_String_canonical Á¤º¸ CC(CS)C(=O)N1CCCC1C(O)=O
Hydrochlorothiazide¿¡ ´ëÇÑ Smiles_String_canonical Á¤º¸ NS(=O)(=O)C1=C(Cl)C=C2NCNS(=O)(=O)C2=C1
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| Smiles String Isomeric |
Captopril¿¡ ´ëÇÑ Smiles_String_isomeric Á¤º¸ C[C@H](CS)C(=O)N1CCC[C@H]1C(O)=O
Hydrochlorothiazide¿¡ ´ëÇÑ Smiles_String_isomeric Á¤º¸ NS(=O)(=O)C1=C(Cl)C=C2NCNS(=O)(=O)C2=C1
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| InChI Identifier |
Captopril¿¡ ´ëÇÑ InChI_Identifier Á¤º¸ InChI=1/C9H15NO3S/c1-6(5-14)8(11)10-4-2-3-7(10)9(12)13/h6-7,14H,2-5H2,1H3,(H,12,13)/t6-,7+/m1/s1/f/h12H
Hydrochlorothiazide¿¡ ´ëÇÑ InChI_Identifier Á¤º¸ InChI=1/C7H8ClN3O4S2/c8-4-1-5-7(2-6(4)16(9,12)13)17(14,15)11-3-10-5/h1-2,10-11H,3H2,(H2,9,12,13)/f/h9H2
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| Chemical IUPAC Name |
Captopril¿¡ ´ëÇÑ Chemical_IUPAC_Name Á¤º¸ (2S)-1-[(2S)-2-methyl-3-sulfanylpropanoyl]pyrrolidine-2-carboxylic acid
Hydrochlorothiazide¿¡ ´ëÇÑ Chemical_IUPAC_Name Á¤º¸ 6-chloro-1,1-dioxo-3,4-dihydro-2H-benzo[e][1,2,4]thiadiazine-7-sulfonamide
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| Drug-Induced Toxicity Related Proteins |
CAPTOPRIL ÀÇ Drug-Induced Toxicity Related ProteinÁ¤º¸ Replated Protein:Lysozyme Drug:captopril Toxicity:peripheral leukopenia. [¹Ù·Î°¡±â] Replated Protein:Angiotensin-converting enzyme Drug:captopril Toxicity:reversible proteinuria. [¹Ù·Î°¡±â] Replated Protein:Beta-glucuronidase Drug:Captopril Toxicity:peripheral leukopenia. [¹Ù·Î°¡±â] Replated Protein:Kallikrein Drug:captopril Toxicity:decreased significantly blood pressure. [¹Ù·Î°¡±â] Replated Protein:Glucose transporter II Drug:captopril Toxicity:resultant ill effects. [¹Ù·Î°¡±â] Replated Protein:B2 bradykinin receptor Drug:Captopril Toxicity:cough. [¹Ù·Î°¡±â] Replated Protein:Glucose transporter I Drug:captopril Toxicity:resultant ill effects. [¹Ù·Î°¡±â] Replated Protein:Angiotensin-converting enzyme(ACE) Drug:Captopril Toxicity:blood-pressure reduction and reduction in left ventricular mass. [¹Ù·Î°¡±â]
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ÃÖ±ÙÁ¤º¸¼öÁ¤ÀÏ 2023-06-02
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º» ¼öÁ¤ÀÏ Á¤º¸´Â Çã°¡Á¤º¸ ÀÌ¿ÜÀÇ ±âŸÁ¤º¸ ¼öÁ¤ÀÏÀ» ÀǹÌÇϹǷÎ, Çã°¡Á¤º¸¼öÁ¤ÀÏÀº º»¹®¿¡ Ç¥±âµÈ ³¯Â¥¸¦ ÂüÁ¶ÇϽñ⠹ٶø´Ï´Ù.
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µå·°ÀÎÆ÷ ÀǾàÇмúÁ¤º¸´Â ½ÄǰÀǾàǰ¾ÈÀüóÀÇ Á¦Ç°Çã°¡»çÇ×, Çмú¹®Çå, Á¦¾àȸ»ç Á¦°øÁ¤º¸ µîÀ» ±Ù°Å·Î ÀÛ¼ºµÈ Âü°í Á¤º¸ÀÔ´Ï´Ù.
Á¤º¸ÀÇ Á¤È®¼ºÀ» À§ÇØ ³ë·ÂÇϰí ÀÖÀ¸³ª ÆíÁý»óÀÇ ¿À·ù, Çã°¡»çÇ× º¯°æ, Ãß°¡ÀûÀÎ Çмú¿¬±¸ ¶Ç´Â Àӻ󿬱¸ ¹ßÇ¥ µîÀ¸·Î ÀÎÇØ ¹ß»ýÇÏ´Â ¹®Á¦¿¡ ´ëÇØ µå·°ÀÎÆ÷´Â
Ã¥ÀÓÀ» ÁöÁö ¾Ê½À´Ï´Ù. ÀÚ¼¼ÇÑ ³»¿ëÀº ¡°Ã¥ÀÓÀÇ ÇÑ°è ¹× ¹ýÀû°íÁö¡±¸¦ ÂüÁ¶ÇØ ÁֽʽÿÀ.
¹Ýµå½Ã Á¦Á¶¡¤¼öÀÔ»ç, ÆÇ¸Å»ç, ÀÇ»ç, ¾à»ç¿¡°Ô ÃÖÁ¾ÀûÀ¸·Î È®ÀÎÇϽñ⠹ٶø´Ï´Ù.
ÀüÈ: 02-3486-1061 ¤Ó À̸ÞÀÏ: webmaster@druginfo.co.kr
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