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(atenolol Dµî±Þ. ChlorthalidoneÀº Àӽżº °íÇ÷¾Ð¿¡ Åõ¿©½Ã Dµî±Þ. )
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Atenolol¿¡ ´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 |
Atenolol¿¡ ´ëÇÑ Mechanism_Of_Action Á¤º¸ Like metoprolol, atenolol competes with sympathomimetic neurotransmitters such as catecholamines for binding at beta(1)-adrenergic receptors in the heart and vascular smooth muscle, inhibiting sympathetic stimulation. This results in a reduction in resting heart rate, cardiac output, systolic and diastolic blood pressure, and reflex orthostatic hypotension. Higher doses of atenolol also competitively block beta(2)-adrenergic responses in the bronchial and vascular smooth muscles.
Chlorthalidone¿¡ ´ëÇÑ Mechanism_Of_Action Á¤º¸ Chlorthalidone inhibits sodium ion transport across the renal tubular epithelium in the cortical diluting segment of the ascending limb of the loop of Henle. By increasing the delivery of sodium to the distal renal tubule, Chlorthalidone indirectly increases potassium excretion via the sodium-potassium exchange mechanism.
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| Pharmacology |
Atenolol¿¡ ´ëÇÑ Pharmacology Á¤º¸ Atenolol, a competitive beta(1)-selective adrenergic antagonist, has the lowest lipid solubility of this drug class. Although it is similar to metoprolol, atenolol differs from pindolol and propranolol in that it does not have intrinsic sympathomimetic properties or membrane-stabilizing activity. Atenolol is used alone or with chlorthalidone in the management of hypertension and edema.
Chlorthalidone¿¡ ´ëÇÑ Pharmacology Á¤º¸ Chlorthalidone, a monosulfonamyl diuretic, differs form other thiazide diuretics in that a double ring system is incorporated into its structure. Chlorthalidone is used alone or with atenolol in the management of hypertension and edema.
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| Metabolism |
Atenolol¿¡ ´ëÇÑ Metabolism Á¤º¸ # Phase_1_Metabolizing_Enzyme:Cytochrome P450 2D6 (CYP2D6)
Chlorthalidone¿¡ ´ëÇÑ Metabolism Á¤º¸ # Phase_1_Metabolizing_Enzyme:Not Available
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| Protein Binding |
Atenolol¿¡ ´ëÇÑ ´Ü¹é°áÇÕ Á¤º¸ Plasma protein binding is 6-16%
Chlorthalidone¿¡ ´ëÇÑ ´Ü¹é°áÇÕ Á¤º¸ High (75% [58% to albumin])
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| Half-life |
Atenolol¿¡ ´ëÇÑ ¹Ý°¨±â Á¤º¸ 6-7 hours
Chlorthalidone¿¡ ´ëÇÑ ¹Ý°¨±â Á¤º¸ 40 hours
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| Absorption |
Atenolol¿¡ ´ëÇÑ Absorption Á¤º¸ Approximately 50% of an oral dose is absorbed from the gastrointestinal tract, the remainder being excreted unchanged in the feces.
Chlorthalidone¿¡ ´ëÇÑ Absorption Á¤º¸ Absorbed relatively rapidly after oral administration.
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| Pharmacokinetics |
AtenololÀÇ ¾à¹°µ¿·ÂÇÐÀÚ·á
- Èí¼ö : À§Àå°ü¿¡¼ Èí¼ö°¡ ºÒ¿ÏÀüÇÏ´Ù.
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| Biotransformation |
Atenolol¿¡ ´ëÇÑ Biotransformation Á¤º¸ Hepatic (minimal)
Chlorthalidone¿¡ ´ëÇÑ Biotransformation Á¤º¸ Liver
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| Toxicity |
Atenolol¿¡ ´ëÇÑ Toxicity Á¤º¸ LD50=2000-3000 mg/kg(orally in mice). Symptoms of an atenolol overdose include a slow heart beat, shortness of breath, fainting, dizziness, weakness, confusion, nausea, and vomiting.
Chlorthalidone¿¡ ´ëÇÑ Toxicity Á¤º¸ Symptoms of overdose include nausea, weakness, dizziness and disturbances of electrolyte balance.
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| Drug Interactions |
Atenolol¿¡ ´ëÇÑ Drug_Interactions Á¤º¸ Acetohexamide The beta-blocker decreases the symptoms of hypoglycemiaAmpicillin Ampicillin decreases bioavailability of atenololChlorpropamide The beta-blocker decreases the symptoms of hypoglycemiaClonidine Increased hypertension when clonidine stoppedDihydroergotamine Ischemia with risk of gangreneDihydroergotoxine Ischemia with risk of gangreneDiltiazem Increased risk of bradycardiaDisopyramide The beta-blocker increases toxicity of disopyramideEpinephrine Hypertension, then bradycardiaErgonovine Ischmeia with risk of gangreneErgotamine Ischemia with risk of gangreneFenoterol AntagonismFormoterol AntagonismGliclazide The beta-blocker decreases the symptoms of hypoglycemiaGlipizide The beta-blocker decreases the symptoms of hypoglycemiaGlisoxepide The beta-blocker decreases the symptoms of hypoglycemiaGlibenclamide The beta-blocker decreases the symptoms of hypoglycemiaGlycodiazine The beta-blocker decreases the symptoms of hypoglycemiaIbuprofen Risk of inhibition of renal prostaglandinsIndomethacin Risk of inhibition of renal prostaglandinsInsulin The beta-blocker decreases the symptoms of hypoglycemiaInsulin-aspart The beta-blocker decreases the symptoms of hypoglycemiaInsulin-glargine The beta-blocker decreases the symptoms of hypoglycemiaInsulin-detemir The beta-blocker decreases the symptoms of hypoglycemiaInsulin-glulisine The beta-blocker decreases the symptoms of hypoglycemiaInsulin-lispro The beta-blocker decreases the symptoms of hypoglycemiaIsoproterenol AntagonismLidocaine The beta-blocker increases the effect and toxicity of lidocaineMethysergide Ischemia with risk of gangreneOrciprenaline AntagonismPirbuterol AntagonismPiroxicam Risk of inhibition of renal prostaglandinsPrazosin Risk of hypotension at the beginning of therapyProcaterol AntagonismRepaglinide The beta-blocker decreases the symptoms of hypoglycemiaSalbutamol AntagonismSalmeterol AntagonismTerbutaline AntagonismTolazamide The beta-blocker decreases the symptoms of hypoglycemiaTolbutamide The beta-blocker decreases the symptoms of hypoglycemiaVerapamil Increased effect of both drugs
Chlorthalidone¿¡ ´ëÇÑ Drug_Interactions Á¤º¸ Amantadine The diuretic increases the adverse effects of amantadineDeslanoside Possible electrolyte variations and arrhythmiasDiazoxide Significant hyperglycemic effectDigitoxin Possible electrolyte variations and arrhythmiasDigoxin Possible electrolyte variations and arrhythmiasDofetilide Increased risk of cardiotoxicity and arrythmiasLithium The thiazide diuretic increases serum levels of lithium
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CYP450 Drug Interaction |
[CYP450 TableÁ÷Á¢Á¶È¸]
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| Food Interaction |
Atenolol¿¡ ´ëÇÑ Food Interaction Á¤º¸ Consult your doctor before taking large amounts of Vitamin K (Green leafy vegetables).Take 30-60 minutes before meals, take at the same time each day.
Chlorthalidone¿¡ ´ëÇÑ Food Interaction Á¤º¸ Take with food (increases availability).
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| Drug Target |
[Drug Target]
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| Description |
Atenolol¿¡ ´ëÇÑ Description Á¤º¸ A cardioselective beta-adrenergic blocker possessing properties and potency similar to propranolol, but without a negative inotropic effect. [PubChem]
Chlorthalidone¿¡ ´ëÇÑ Description Á¤º¸ A benzenesulfonamide-phthalimidine that tautomerizes to a benzophenones form. It is considered a thiazide-like diuretic. [PubChem]
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| Drug Category |
Atenolol¿¡ ´ëÇÑ Drug_Category Á¤º¸ Adrenergic AgentsAdrenergic beta-AntagonistsAnti-Arrhythmia AgentsAntiarrhythmic AgentsAntihypertensive AgentsSympatholytics
Chlorthalidone¿¡ ´ëÇÑ Drug_Category Á¤º¸ Antihypertensive AgentsDiureticsSodium Chloride Symporter Inhibitors
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| Smiles String Canonical |
Atenolol¿¡ ´ëÇÑ Smiles_String_canonical Á¤º¸ CC(C)NCC(O)COC1=CC=C(CC(N)=O)C=C1
Chlorthalidone¿¡ ´ëÇÑ Smiles_String_canonical Á¤º¸ NS(=O)(=O)C1=C(Cl)C=CC(=C1)C1(O)NC(=O)C2=CC=CC=C12
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| Smiles String Isomeric |
Atenolol¿¡ ´ëÇÑ Smiles_String_isomeric Á¤º¸ CC(C)NC[C@@H](O)COC1=CC=C(CC(N)=O)C=C1
Chlorthalidone¿¡ ´ëÇÑ Smiles_String_isomeric Á¤º¸ NS(=O)(=O)C1=C(Cl)C=CC(=C1)[C@@]1(O)NC(=O)C2=CC=CC=C12
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| InChI Identifier |
Atenolol¿¡ ´ëÇÑ InChI_Identifier Á¤º¸ InChI=1/C14H22N2O3/c1-10(2)16-8-12(17)9-19-13-5-3-11(4-6-13)7-14(15)18/h3-6,10,12,16-17H,7-9H2,1-2H3,(H2,15,18)/f/h15H2
Chlorthalidone¿¡ ´ëÇÑ InChI_Identifier Á¤º¸ InChI=1/C14H11ClN2O4S/c15-11-6-5-8(7-12(11)22(16,20)21)14(19)10-4-2-1-3-9(10)13(18)17-14/h1-7,19H,(H,17,18)(H2,16,20,21)/f/h17H,16H2
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| Chemical IUPAC Name |
Atenolol¿¡ ´ëÇÑ Chemical_IUPAC_Name Á¤º¸ 2-[4-[2-hydroxy-3-(propan-2-ylamino)propoxy]phenyl]acetamide
Chlorthalidone¿¡ ´ëÇÑ Chemical_IUPAC_Name Á¤º¸ 2-chloro-5-(1-hydroxy-3-oxo-2H-isoindol-1-yl)benzenesulfonamide
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| Drug-Induced Toxicity Related Proteins |
ATENOLOL ÀÇ Drug-Induced Toxicity Related ProteinÁ¤º¸ Replated Protein:CYP2D6 Drug:Atenolol Toxicity:Increased beta-blockade. [¹Ù·Î°¡±â]
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ÀüÈ: 02-3486-1061 ¤Ó À̸ÞÀÏ: webmaster@druginfo.co.kr
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The database contains the following fields: The generic name of each chemical For module A10 (liver enzyme composite module): Overall activity category for each compound (A for active, M for marginally active, or I for inactive) based on the number of active and marginally active scores for each compound at the five individual endpoints (see research article for full description of method) Number of endpoints at which each compound is marginally active (M) Number of endpoints at which each compound is active (A) For modules A11 to A15 (alkaline phosphatase increased, SGOT increased, SGPT increased, LDH increased, and GGT increased, respectively): Overall activity category for each compound (A for active, M for marginally active, or I for inactive) based on the RI and ADR values (see the research article for full description of method) Number of ADR reports for each compound, given as <4 or ¡Ã4 Reporting Index value for each compound, except where no shipping units were available (NSU) Group 1 comprises of compounds for which ADR data were available for the first five years of marketing, so when no ADR reports were listed during this period the compounds were evaluated as inactive. Group 2 comprises of compounds for which a 'steady state' period of ADR data were available (1992-1996). In cases where no ADR reports were filed during this period, the compounds were scored as 'NA' (data not available) since they may have had one or more ADR reports during their first five years of marketing which should not be negated by a lack of ADR reports during the steady-state period. ATENOLOL[GGT Increase][Composite Activity](Score) I(Marginal) 0(Active) 0[Alkaline Phosphatase Increase](Activity Score) I(Number of Rpts) <4(Index value) 0.1[SGOT Increase](Activity Score) I(Number of Rpts) ¡Ã4(Index value) 0.5[SGPT Increase](Activity Score) I(Number of Rpts) ¡Ã4(Index value) 0.3[LDH Increase](Activity Score) I(Number of Rpts) <4(Index value) 0.1[GGT Increase](Activity Score) I(Number of Rpts) <4(Index value) 0
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