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| Mechanism of Action |
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.
Olmesartan¿¡ ´ëÇÑ Mechanism_Of_Action Á¤º¸ Angiotensin II is formed from angiotensin I in a reaction catalyzed by angiotensin converting enzyme (ACE, kininase II). Angiotensin II is the principal pressor agent of the renin-angiotensin system, with effects that include vasoconstriction, stimulation of synthesis and release of aldosterone, cardiac stimulation and renal reabsorption of sodium. Olmesartan blocks the vasoconstrictor effects of angiotensin II by selectively blocking the binding of angiotensin II to the AT1 receptor in vascular smooth muscle. Its action is, therefore, independent of the pathways for angiotensin II synthesis. Olmesartan has more than a 12,500-fold greater affinity for the AT1 receptor than for the AT2 receptor.
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| Pharmacology |
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.
Olmesartan¿¡ ´ëÇÑ Pharmacology Á¤º¸ Olmesartan, a specific angiotensin II type 1 antagonist, is used alone or with other antihypertensive agents to treat hypertension. Unlike the angiotensin receptor antagonist losartan, olmesartan does not have an active metabolite or possess uricosuric effects. Blockade of the angiotensin II receptor inhibits the negative regulatory feedback of angiotensin II on renin secretion, but the resulting increased plasma renin activity and circulating angiotensin II levels do not overcome the effect of olmesartan on blood pressure.
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| Metabolism |
Hydrochlorothiazide¿¡ ´ëÇÑ Metabolism Á¤º¸ # Phase_1_Metabolizing_Enzyme:Not Available
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| Absorption |
Hydrochlorothiazide¿¡ ´ëÇÑ Absorption Á¤º¸ 50-60%
Olmesartan¿¡ ´ëÇÑ Absorption Á¤º¸ Bioavailability is about 26%. Food does not affect the bioavailability of olmesartan.
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| Pharmacokinetics |
Olmesartan medoxomilÀÇ ¾à¹°µ¿·ÂÇÐÀÚ·á
¡Ü Absorption
°æ±¸Á¦Á¦ÀÇ »ýüÀÌ¿ë·ü(F) :26%
À½½ÄÀº olmesaltanÀÇ Èí¼ö¿¡ ¿µÇâÀ» ¹ÌÄ¡Áö ¾Ê´Â´Ù.
¡Ü Distribution
ÃÑ ´Ü¹é°áÇÕ·ü: 99%
ŹÝÀ» Åë°úÇÏ¿© žƿ¡ ºÐÆ÷µÊ.
¡Ü Metabolism
Olmesartan medoxomil´Â À庮¿¡¼ 100% olmesartanÀÇ È°¼ºÇüÀ¸·Î º¯ÈµÈ´Ù. (cytochrome P450È¿¼Ò±º°ú °ü·Ã ¾øÀ½)
¡Ü Excretion
µ¿¹°½ÇÇè¿¡¼´Â ¼öÀ¯½Ã ¸ðÀ¯·Î ¹è¼³ÀÌ µÈ °ÍÀÌ º¸°í µÇ¾úÀ¸³ª »ç¶÷¿¡¼´Â ¾Ë·ÁÁöÁö ¾Ê¾Ò´Ù.
½ÅÀå¹è¼³ : 35~50%
´ë»ç¹ÞÀº Ȱ¼ºÇü olmesartanÀÇ ¹Ý°¨±â : 12~18½Ã°£
¡Ü onset : 1ÁÖ
¡Ü duration : 2~4ÁÖ
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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| Toxicity |
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.
Olmesartan¿¡ ´ëÇÑ Toxicity Á¤º¸ Symptoms of overdose include dehydration (dry mouth, excessive thirst, muscle pain or cramps, nausea and vomiting, weakness), dizziness, low blood pressure, and slow or irregular heartbeat.
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| Drug Interactions |
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
Olmesartan¿¡ ´ëÇÑ Drug_Interactions Á¤º¸ Drospirenone Increased risk of hyperkaliemia
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CYP450 Drug Interaction |
[CYP450 TableÁ÷Á¢Á¶È¸]
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| Food Interaction |
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.
Olmesartan¿¡ ´ëÇÑ Food Interaction Á¤º¸ Food does not affect the bioavailability of olmesartan.
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| Drug Target |
[Drug Target]
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| Description |
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]
Olmesartan¿¡ ´ëÇÑ Description Á¤º¸ Olmesartan belongs to the class of medicines called angiotensin II receptor antagonists to treat high blood pressure. It is marketed worldwide by Daiichi Sankyo, Ltd. and in the United States by Daiichi Sankyo, Inc. and Forest Laboratories.
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| Dosage Form |
Olmesartan¿¡ ´ëÇÑ Dosage_Form Á¤º¸ Tablet Oral
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| Drug Category |
Hydrochlorothiazide¿¡ ´ëÇÑ Drug_Category Á¤º¸ Antihypertensive AgentsDiureticsSodium Chloride Symporter Inhibitors
Olmesartan¿¡ ´ëÇÑ Drug_Category Á¤º¸ Angiotensin II Type 1 Receptor BlockersAntihypertensive Agents
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| Smiles String Canonical |
Hydrochlorothiazide¿¡ ´ëÇÑ Smiles_String_canonical Á¤º¸ NS(=O)(=O)C1=C(Cl)C=C2NCNS(=O)(=O)C2=C1
Olmesartan¿¡ ´ëÇÑ Smiles_String_canonical Á¤º¸ CCCC1=NC(=C(N1CC1=CC=C(C=C1)C1=CC=CC=C1C1=NNN=N1)C(=O)OCC1=C(C)OC(=O)O1)C(C)(C)O
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| Smiles String Isomeric |
Hydrochlorothiazide¿¡ ´ëÇÑ Smiles_String_isomeric Á¤º¸ NS(=O)(=O)C1=C(Cl)C=C2NCNS(=O)(=O)C2=C1
Olmesartan¿¡ ´ëÇÑ Smiles_String_isomeric Á¤º¸ CCCC1=NC(=C(N1CC1=CC=C(C=C1)C1=CC=CC=C1C1=NNN=N1)C(=O)OCC1=C(C)OC(=O)O1)C(C)(C)O
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| InChI Identifier |
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
Olmesartan¿¡ ´ëÇÑ InChI_Identifier Á¤º¸ InChI=1/C29H30N6O6/c1-5-8-23-30-25(29(3,4)38)24(27(36)39-16-22-17(2)40-28(37)41-22)35(23)15-18-11-13-19(14-12-18)20-9-6-7-10-21(20)26-31-33-34-32-26/h6-7,9-14,38H,5,8,15-16H2,1-4H3,(H,31,32,33,34)/f/h33H
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| Chemical IUPAC Name |
Hydrochlorothiazide¿¡ ´ëÇÑ Chemical_IUPAC_Name Á¤º¸ 6-chloro-1,1-dioxo-3,4-dihydro-2H-benzo[e][1,2,4]thiadiazine-7-sulfonamide
Olmesartan¿¡ ´ëÇÑ Chemical_IUPAC_Name Á¤º¸ (5-methyl-2-oxo-1,3-dioxol-4-yl)methyl 5-(2-hydroxypropan-2-yl)-2-propyl-3-[[4-[2-(2H-tetrazol-5-yl)phenyl]phenyl]methyl]imidazole-4-carboxylate
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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
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ÀüÈ: 02-3486-1061 ¤Ó À̸ÞÀÏ: webmaster@druginfo.co.kr
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