Gastric mucosal protection by acetazolamide derivatives: Role of carbonic anhydrase and sulfhydryls
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Acetazolamide
Sulfanilamide
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N-Substituted sulfonamide carbonic anhydrase inhibitors with topical effects on intraocular pressure
ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTN-Substituted sulfonamide carbonic anhydrase inhibitors with topical effects on intraocular pressureMichael W. Duffel, I. Silwai Ing, Tyrone M. Segarra, John A. Dixson, Charles F. Barfknecht, and Ronald D. SchoenwaldCite this: J. Med. Chem. 1986, 29, 8, 1488–1494Publication Date (Print):August 1, 1986Publication History Published online1 May 2002Published inissue 1 August 1986https://pubs.acs.org/doi/10.1021/jm00158a028https://doi.org/10.1021/jm00158a028research-articleACS PublicationsRequest reuse permissionsArticle Views786Altmetric-Citations41LEARN ABOUT THESE METRICSArticle Views are the COUNTER-compliant sum of full text article downloads since November 2008 (both PDF and HTML) across all institutions and individuals. These metrics are regularly updated to reflect usage leading up to the last few days.Citations are the number of other articles citing this article, calculated by Crossref and updated daily. Find more information about Crossref citation counts.The Altmetric Attention Score is a quantitative measure of the attention that a research article has received online. Clicking on the donut icon will load a page at altmetric.com with additional details about the score and the social media presence for the given article. Find more information on the Altmetric Attention Score and how the score is calculated. Share Add toView InAdd Full Text with ReferenceAdd Description ExportRISCitationCitation and abstractCitation and referencesMore Options Share onFacebookTwitterWechatLinked InRedditEmail Other access optionsGet e-Alertsclose Get e-Alerts
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The possible role of carbonic anhydrase in bone resorption induced by prostaglandin E2 (PGE2) was studied using an in vitro neonatal mouse calvarial culture system. PGE2 (10–6M) was effective in stimulating resorption, as assessed by calcium release into culture media. This enhanced resorption was accompanied by significant increases in calvarial carbonic anhydrase activity over control values at 48 and 96 h. At 48 h, bones treated with PGE2 had 20% more carbonic anhydrase activity than controls. By 96 h, treated bones contained 79% more carbonic anhydrase activity than controls. PGE2-induced bone resorption was inhibited by the carbonic anhydrase inhibitor acetazolamide in a dose-dependent fashion from 10–5 to 10–4M, with 77% inhibition observed at 10–4M. The acetazolamide analogue CL 13,850 (N-t-butylacetazolamide), which does not inhibit carbonic anhydrase, failed to inhibit PGE2-induced resorption. These results are consistent with the hypothesis that carbonic anhydrase is a necessary component of the osteoclastic bone resorptive mechanism.
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Four carbonic anhydrase inhibitors (acetazolamide, dichlorphenamide, ethoxzolamide, and methazolamide) cause ocular hypotony in normotensive and glaucomatous Beagles. Four dosages of acetazolamide and methazolamide and three dosages of dichlorphenamide and ethoxzolamide were evaluated. The extent of ocular hypotony after these carbonic anhydrase inhibitors was usually greater in glaucomatous Beagles than it was in normotensive Beagles.
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Carbonic anhydrase(CA) can catalyze hydration reaction of carbon dioxide reversibly,and produce H+ and HCO3-that take part in multi-physiologic function.The α-CA's isozymes(CA I,CA II,CA IV,CA IX and CA XII) have been much more studied.Acetazolamide,one of the important CA inhibitors,has been used clinically for a long time.It has been used for the treatment of cardiac edema and glaucoma,and has no practical value on these diseases because of its frequent side effects.Recently,researchers have found that acetazolamide has a broad spectrum of inhibiting carbonic anhydrase in many tissues and cells.It disrupts the positive hydration reaction of carbon dioxide,and has beneficial effect on biochemical metabolic disorder in various pathologic states.Therefore,a number of new clinical applications of acetazolamide have been developed.In this article,we reviewed the recent progress in clinical applications of acetazolamide,such as for treatments of acute high altitude sickness,chronic mountain sickness,cerebrovascular disease,tumor,refractory hiccough,epilepsy,metabolic bone disease,and hyperbaric oxygen-induced convulsion.
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We examined the relative potencies of zonisamide (CAS 68291-97-4) to acetazolamide in inhibiting carbonic anhydrases in human erythrocytes and purified human carbonic anhydrase I and II in vitro and found them to be about 1/150, 1/8 and 1/188, respectively. The IC50 values of zonisamide and acetazolamide for the inhibition of erythrocyte enzymes were close to those of purified carbonic anhydrase II. This result indicates that zonisamide actually differs from acetazolamide in their actions on the physiological events which are coupled with CO2 hydration in vivo.
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This study investigated the inhibitory effect of a high efficiency diuretic, furosemide, on carbonic anhydrase (CA). First, comparing the inhibitory effect of acetazolamide, a low efficiency diuretic, on CA, shows that furosemide or acetazolamide can quickly make CA inactive when its concentration is close to the enzyme concentration, different from the usual inhibitory kinetics in which the concentration of the inhibitor is far higher than the enzyme concentration. Secondly, the reaction of the enzyme indicates that the inhibitory effect of furosemide or acetazolamide on carbonic anhydrase is quickly reversible. Finally, the degree of the inhibitory effect of furosemide and of acetazolamide on CA are compared. The results show that furosemide inhibits CA less than acetazolamide.
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1. We considered whether some of the carbonic anhydrase of the lung is on the surface of the pulmonary capillaries so that it acts directly on plasma as it traverses the pulmonary capillaries to accelerate CO2/pH equilibration. 2. Experiments were performed on spontaneously breathing cats or saline-perfused cat lungs. 3. In intact cats, Tris buffer injected suddenly into the right atrium transiently lowered end-tidal CO2, FET, CO2. The rate of CO2 uptake came within an order of magnitude of taxing the calculated diffusing capacity of the lungs. The fall in FET, CO2 was much reduced by giving the carbonic anhydrase inhibitors benzolamide or acetazolamide intravenously, or even by adding benzolamide to the injected Tris. The fall in FET, CO2 could be increased by adding carbonic anhydrase to the injected Tris. 4. In saline-perfused lungs ventilated with 5% CO2 in O2, Tris or alkalinized albumin solution injected into the pulmonary artery transiently lowered FET, CO2 and the effect was reduced by the addition of benzolamide or acetazolamide to the injectate. Injecting Tris bubbled with 15% CO2 caused a rise in FET, CO2, also reduced by benzolamide. 5. We conclude that pulmonary carbonic anhydrase is readily accessible to large or small molecular wight buffers in the capillaries and to inhibitors, and we suggest that it is located on the luminal surface of the capillary endothelium.
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The kinetics of inhibition by acetazolamide and sulfanilamide of the formation of carbon dioxide from bicarbonate, catalyzed by partially purified carbonic an-hydrase preparations from bovine erythrocytes, were those of competitive inhibition. This is contrasted with the non-competitive kinetics of sulfonamide inhibition of a number of carbonic anhydrase-mediated hydration reactions. K1 for acetazolamide was 8.6 × 10-8 M while that for sulfanilamide was 1.8 × 10-5 M; these values are similar to those reported for inhibition of CO2 hydration in the presence of bovine erythrocyte enzyme.
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Abstract The effect of acetazolamide upon the in vivo CO 2 buffer capacity of rat brain tissue was investigated by injecting the animals with the drug in two doses of 50 mg/kg each before they were anesthetized and subsequently exposed to various CO 2 tensions for 40–60 min. Acetazolamide was found to give a marked lowering of the CO 2 buffer capacity. Thus, the intracellular buffer capacity, calculated as β=Δlog pCO 2 /ΔpHi, was found to be about 1.4, and thus considerably lower than the intracellular CO 2 buffer capacity of animals not given acetazolamide but otherwise treated in an identical way (β= 2.3, see Kjällquist, Nardini and Siesjö 1969 a). The results indicate that acetazolamide interferes with an active transport of hydrogen ions between cells and the extracellular fluids which is dependent on carbonic anhydrase.
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Carbonic anhydrase in the red blood cell and in the pulmonary endothelium facilitates the elimination of CO2 in the lungs. Although a carbonic anhydrase inhibitor, such as acetazolamide which is frequently used in patients with glaucoma or with metabolic alkalosis, is known to impair the CO2 elimination in the lungs, the dose-response curve of CO2 elimination with acetazolamide has not been well documented in CO2 homeostasis. In the present study, the effects of inhibited carbonic anhydrase were tested in 8 anesthetized dogs; various dosages of acetazolamide were used. When the administered clinical dosage of acetazolamide increased from 5 to 20mg/kg, PaCO2, PvCO2, arterial-alveolar PCO2 difference (a-ADCO2), and physiological VD/VT ratio increased progressively to 52.0±2.1Torr, 58.0±3.0Torr, 23.4±1.2Torr, and by 19.2±1.8% (S.E.) respectively, whereas inhibition rate of red blood cell carbonic anhydrase (RCA) activity increased progressively to 73.1±2.1% (S.E.). On the other hand, PACO2 decreased to 27.1±1.8Torr (S.E.) upon the first injection of 5mg/kg of acetazolamide, but PACO2 did not change further upon 3 additional 5mg/kg injections. Mixed venous-arterial PCO2 difference ((v-a)PCO2), VCO2, and anatomical VD/VT ratio were unchanged by the administration of any doses of acetazolamide.
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