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Namespace Prefixes

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Statements

Subject Item
n2:DB00606
rdf:type
n3:Drug
n3:description
As a diuretic, cyclothiazide 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 cyclothiazide 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 cyclothiazide 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. Cyclothiazide is indicated as adjunctive therapy in edema associated with congestive heart failure, hepatic cirrhosis, and corticosteroid and estrogen therapy. It is also indicated in the management of hypertension either as the sole therapeutic agent or to enhance the effectiveness of other antihypertensive drugs in the more severe forms of hypertension.
n3:group
approved
n3:indication
Cyclothiazide is indicated as adjunctive therapy in edema associated with congestive heart failure, hepatic cirrhosis, and corticosteroid and estrogen therapy. It is also indicated in the management of hypertension either as the sole therapeutic agent or to enhance the effectiveness of other antihypertensive drugs in the more severe forms of hypertension.
n3:manufacturer
n5:271B5508-363D-11E5-9242-09173F13E4C5 n5:271B5509-363D-11E5-9242-09173F13E4C5
owl:sameAs
n8:DB00606 n13:DB00606
dcterms:title
Cyclothiazide
adms:identifier
n12:50192229 n14:46508269 n15:DB00606 n16:C12685 n17:31448 n18:2807 n19:PA449168 n20:2910 n23:D01256 n24:CYZ
n3:mechanismOfAction
Hydrochlorothiazide, a thiazide diuretic, inhibits water reabsorption in the nephron by inhibiting the sodium-chloride symporter (SLC12A3) in the distal convoluted tubule, which is responsible for 5% of total sodium reabsorption. Normally, the sodium-chloride symporter transports sodium and chloride from the lumen into the epithelial cell lining the distal convoluted tubule. The energy for this is provided by a sodium gradient established by sodium-potassium ATPases on the basolateral membrane. Once sodium has entered the cell, it is transported out into the basolateral interstitium via the sodium-potassium ATPase, causing an increase in the osmolarity of the interstitium, thereby establishing an osmotic gradient for water reabsorption. By blocking the sodium-chloride symporter, hydrochlorothiazide effectively reduces the osmotic gradient and water reabsorption throughout the nephron.Hydrochlorothiazide, a thiazide diuretic, inhibits water reabsorption in the nephron by inhibiting the sodium-chloride symporter (SLC12A3) in the distal convoluted tubule, which is responsible for 5% of total sodium reabsorption. Normally, the sodium-chloride symporter transports sodium and chloride from the lumen into the epithelial cell lining the distal convoluted tubule. The energy for this is provided by a sodium gradient established by sodium-potassium ATPases on the basolateral membrane. Once sodium has entered the cell, it is transported out into the basolateral interstitium via the sodium-potassium ATPase, causing an increase in the osmolarity of the interstitium, thereby establishing an osmotic gradient for water reabsorption. By blocking the sodium-chloride symporter, hydrochlorothiazide effectively reduces the osmotic gradient and water reabsorption throughout the nephron.
n3:synonym
Ciclotiazide 6-chloro-3,4-dihydro-3-(2-Norbornen-5-yl)-7-sulfamoyl-1,2,4-benzothiadiazine 1,1-dioxide Cyclothiazidum Cyclothiazide 6-chloro-3-(2-Norbornen-5-yl)-7-sulfamyl-3,4-dihydro-1,2,4-benzothiadiazine 1,1-dioxide 6-chloro-3,4-dihydro-3-(5-Norbornen-2-yl)-2H-1,2,4-benzothiadiazine-7-sulfonamide 1,1-dioxide 6-chloro-3,4-dihydro-3-(2-Norbornen-5-yl)-2H-1,2,4-benzothiadiazine-7-sulfonamide 1,1-dioxide Ciclotiazida
n3:toxicity
Oral LD<sub>50</sub> in mouse is > 10000 mg/kg, and > 4000 mg/kg in rat. Signs of overdose include 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.
n3:synthesisReference
Muller, E. and Hasspacher, K.; US. Patent 3,275,625; September 27,1966; assigned to Boehringer lngelheim GmbH, Germany.
n9:hasConcept
n10:M0045761
n3:IUPAC-Name
n4:271B550E-363D-11E5-9242-09173F13E4C5
n3:InChI
n4:271B5514-363D-11E5-9242-09173F13E4C5
n3:Molecular-Formula
n4:271B5513-363D-11E5-9242-09173F13E4C5
n3:Molecular-Weight
n4:271B5510-363D-11E5-9242-09173F13E4C5
n3:Monoisotopic-Weight
n4:271B5511-363D-11E5-9242-09173F13E4C5
n3:SMILES
n4:271B5512-363D-11E5-9242-09173F13E4C5
n3:Water-Solubility
n4:271B550C-363D-11E5-9242-09173F13E4C5
n3:logP
n4:271B5525-363D-11E5-9242-09173F13E4C5 n4:271B550D-363D-11E5-9242-09173F13E4C5 n4:271B550A-363D-11E5-9242-09173F13E4C5
n3:logS
n4:271B550B-363D-11E5-9242-09173F13E4C5
n21:hasATCCode
n22:C03AA09
n3:H-Bond-Acceptor-Count
n4:271B551A-363D-11E5-9242-09173F13E4C5
n3:H-Bond-Donor-Count
n4:271B551B-363D-11E5-9242-09173F13E4C5
n3:InChIKey
n4:271B5515-363D-11E5-9242-09173F13E4C5
n3:Polar-Surface-Area--PSA-
n4:271B5516-363D-11E5-9242-09173F13E4C5
n3:Polarizability
n4:271B5518-363D-11E5-9242-09173F13E4C5
n3:Refractivity
n4:271B5517-363D-11E5-9242-09173F13E4C5
n3:Rotatable-Bond-Count
n4:271B5519-363D-11E5-9242-09173F13E4C5
n3:affectedOrganism
Humans and other mammals
n3:casRegistryNumber
2259-96-3
n3:category
n3:Bioavailability
n4:271B5520-363D-11E5-9242-09173F13E4C5
n3:Ghose-Filter
n4:271B5522-363D-11E5-9242-09173F13E4C5
n3:MDDR-Like-Rule
n4:271B5523-363D-11E5-9242-09173F13E4C5
n3:Melting-Point
n4:271B5524-363D-11E5-9242-09173F13E4C5
n3:Number-of-Rings
n4:271B551F-363D-11E5-9242-09173F13E4C5
n3:Physiological-Charge
n4:271B551E-363D-11E5-9242-09173F13E4C5
n3:Rule-of-Five
n4:271B5521-363D-11E5-9242-09173F13E4C5
n3:Traditional-IUPAC-Name
n4:271B550F-363D-11E5-9242-09173F13E4C5
n3:pKa--strongest-acidic-
n4:271B551C-363D-11E5-9242-09173F13E4C5
n3:pKa--strongest-basic-
n4:271B551D-363D-11E5-9242-09173F13E4C5