Renal handling of exogenous and metabolic carbon dioxide
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Abstract:
The multiple-indicator-dilution technique has been applied to a study of the permeability of proximal and distal portions of the nephrons to dissolved carbon dioxide and bicarbonate ion in anesthetized dogs. Under control conditions with mannitol loading, the excreted carbon dioxide appears considerably earlier than the simultaneously injected creatinine whether dissolved CO 2 or bicarbonate ion is injected. After inhibition of carbonic anhydrase by acetazolamide, there is relatively little effect on the excretion pattern of dissolved CO 2 . However, the excretion pattern of bicarbonate ion becomes nearly parallel to that of creatinine: the early peak disappears. On the basis of these results, it is concluded that the distal portions of the nephrons are permeable to dissolved CO 2 but impermeable to bicarbonate ion and that, under control conditions, carbonic anhydrase serves to establish a catalytically mediated diffusion exchange for the transfer of CO 2 derived from bicarbonate ion. Similar conclusions may apply to the proximal portions of the nephrons. On taking into account other data, it appears that the collecting ducts are impermeable to dissolved carbon dioxide. Carbon dioxide produced by decarboxylation of pyruvate has excretion patterns similar to those obtained for dissolved carbon dioxide. It is concluded that the decarboxylation product is dissolved CO 2 and not bicarbonate ion.Keywords:
Bicarbonate
Carbonic acid
Decarboxylation
Acetazolamide
Dilution
Acetazolamide
Sulfanilamide
Carbonic anhydrase inhibitor
Carbonic anhydrase II
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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
Sulfonamide
Acetazolamide
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Acetazolamide
Trigeminal Nerve
Carbonic Anhydrase I
Carbonic anhydrase inhibitor
Trigeminal ganglion
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Acetazolamide
Carbonic Anhydrase I
Carbonic anhydrase II
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Sudden oxygenation of a thin film of rat brain homogenate, suspended between the surface of a glass pH-sensitive electrode and a gas-permeable membrane, is accompanied by a fall in pH, which is greater when carbonic anhydrase is inhibited. The result suggests that oxidative decarboxylation yields carbonic acid (HCO3− and H+), which dissociates to form molecular carbon dioxide. Brain carbonic anhydrase facilitates the formation of carbon dioxide from the decarboxylation products.
Decarboxylation
Carbonic acid
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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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Acetazolamide
Bufo marinus
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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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Acetazolamide, an inhibitor of the enzyme carbonic anhydrase (E.C. 4.2.1.1.), causes a unique congenital anomaly characterized by postaxial reduction of the distal portion of the right forelimb. To gain an understanding of the mechanism of teratogenesis, the activity of carbonic anhydrase in sensitive and resistant mouse strains, and its inhibition by acetazolamide, were examined. Differences in teratologic sensitivity were found not to be attributable to differences in maternal or embryonic drug levels. Enzyme inhibition at acetazolamide concentrations ranging between 10(-11) and 10(-5) M did not differ between the mouse strains when adult erythrocytes or day 12 embryos were assayed. However, in day 10 embryos, the period of maximum teratologic susceptibility, a small strain difference was found which suggested that the form of carbonic anhydrase in the susceptible CBA/J strain at this time is somewhat more sensitive to inhibition by acetazolamide than the form found in the resistant SWV strain. The results suggest further that more than one isozyme of carbonic anhydrase may be present in all three samples.
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FIVE years ago, Layton and Hallesy1reported that rats fed acetazolamide in the diet during pregnancy gave birth to offspring in which about 36% had a peculiar but specific postaxial defect confined mainly to the right forepaw. The most common lesion was absence of the fourth and fifth digits and the corresponding metacarpals. At that time, it was not clear to me whether this was due to carbonic anhydrase inhibition or some unknown effect of acetazolamide.2More recently, we have clarified this point, since it appears that all the potent carbonic anhydrase inhibitors, ethoxzolamide,3dichlorphenamide,4methazolamide, and benzolamide (unpublished data by W.M. Layton, W.J. Scott, and T.H.M.) cause identical lesions. The high doses (0.2% to 0.6% in the diet, or several hundred milligrams per kilograms per day) used by Layton and Hallesy1were necessary because of their drug-diet method and the relatively short half life
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