scholarly journals Blood carbonic anhydrase activity—A possible role in the production of acid-base imbalance in children and infants

1963 ◽  
Vol 10 (5) ◽  
pp. 428-441
Author(s):  
A. R. Boutros ◽  
V. R. Woodford
Keyword(s):  
Carbonic Anhydrase ◽  
Carbonic Anhydrase Activity ◽  
Acid Base

Effect of acetazolamide on gas exchange and acid-base control after maximal exercise

1992 ◽  
Vol 72 (1) ◽  
pp. 278-287 ◽  
Author(s):  
J. M. Kowalchuk ◽  
G. J. Heigenhauser ◽  
J. R. Sutton ◽  
N. L. Jones
Keyword(s):  
Carbonic Anhydrase ◽  
Muscle Power ◽  
Inorganic Ions ◽  
Carbonic Anhydrase Activity ◽  
Co2 Production ◽  
Acid Base ◽  
Carbonic Anhydrase Inhibition ◽  
Severe Exercise ◽  
Arterial Plasma ◽  
End Tidal

To investigate the interactions between the systems that contribute to acid-base homeostasis after severe exercise, we studied the effects of carbonic anhydrase inhibition on exchange of strong ions and CO2 in six subjects after 30 s of maximal isokinetic cycling exercise. Each subject exercised on two randomly assigned occasions, a control (CON) condition and 30 min after intravenous injection of 1,000 mg acetazolamide (ACZ) to inhibit blood carbonic anhydrase activity. Leg muscle power output was similar in the two conditions; peak O2 uptake (VO2) after exercise was lower in ACZ (2,119 +/- 274 ml/min) than in CON (2,687 +/- 113, P less than 0.05); peak CO2 production (VCO2) was also lower (2,197 +/- 241 in ACZ vs. 3,237 +/- 87 in CON, P less than 0.05) and was accompanied by an increase in the recovery half-time from 1.7 min in CON to 2.3 min in ACZ. Whereas end-tidal PCO2 was lower in ACZ than in CON, arterial PCO2 (PaCO2) was higher, and a large negative end-tidal-to-arterial difference (less than or equal to 20 Torr) was present in ACZ on recovery. In ACZ, postexercise increases in arterial plasma [Na+] and [K+] were greater but [La-] was lower. Arteriovenous differences across the forearm showed a greater uptake of La- and Cl- in CON than in ACZ. Carbonic anhydrase inhibition with ACZ, in addition to impairing equilibration of the CO2 system to the acid-base challenge of exercise, was accompanied by changes in equilibration of strong inorganic ions. A lowered plasma [La-] was not accompanied by greater uptake of La- by inactive muscle.

Histochemical localization of Na+–K+ ATPase and carbonic anhydrase activity in gills of 17 fish species

1988 ◽  
Vol 66 (11) ◽  
pp. 2398-2405 ◽  
Author(s):  
David M. Conley ◽  
Jon Mallatt
Keyword(s):  
Carbonic Anhydrase ◽  
Atpase Activity ◽  
Carbonic Anhydrase Activity ◽  
Chloride Cells ◽  
Shark Species ◽  
Acid Base ◽  
Pavement Cells ◽  
Leopard Shark ◽  
Biochemical Assays ◽  
Definite Correlation

Activities of two enzymes considered to be involved in NaCl regulation, Na+–K+ ATPase and carbonic anhydrase, were localized in gill epithelia of 14 teleost, 2 agnathan, and 1 shark species through light microscopic histochemistry. Findings were confirmed by use of appropriate inhibitors (ouabain, acetazolamide). Na+–K+ ATPase activity was detected in chloride cells of most marine teleost species (six of eight) and of marine leopard shark and hagfish, but never in freshwater fish gills. In general, this finding agrees with past biochemical assays showing gill Na+–K+ ATPase activity to be highest in marine teleosts. Staining for carbonic anhydrase took one of three patterns among species: gill pavement cells or chloride cells, or both, were stained. Interspecific distribution of these patterns bore little relation to taxonomy or to habitat salinity, although chloride cells of euryhaline teleosts seemed more likely to stain than chloride cells of stenohaline teleosts, freshwater or marine. Given the lack of a definite correlation with salinity, it is concluded that fish gill carbonic anhydrase may not function in NaCl regulation as much as in acid–base regulation; the enzyme's role in preventing systemic pH imbalance is discussed.

Does gill boundary layer carbonic anhydrase contribute to carbon dioxide excretion: a comparison between dogfish (Squalus acanthias) and rainbow trout (Oncorhynchus mykiss)

1999 ◽  
Vol 202 (6) ◽  
pp. 749-756 ◽  
Author(s):  
S.F. Perry ◽  
K.M. Gilmour ◽  
N.J. Bernier ◽  
C.M. Wood
Keyword(s):  
Carbon Dioxide ◽  
Boundary Layer ◽  
Rainbow Trout ◽  
Carbonic Anhydrase ◽  
Carbonic Anhydrase Activity ◽  
Squalus Acanthias ◽  
Stopped Flow ◽  
Acid Base ◽  
Rainbow Trout Oncorhynchus Mykiss ◽  
Co2 Excretion

In vivo experiments were conducted on spiny dogfish (Squalus acanthias) and rainbow trout (Oncorhynchus mykiss) in sea water to determine the potential role of externally oriented or gill boundary layer carbonic anhydrase in carbon dioxide excretion. This was accomplished by assessing pH changes in expired water using a stopped-flow apparatus. In dogfish, expired water was in acid-base disequilibrium as indicated by a pronounced acidification (delta pH=−0.11+/−0.01; N=22; mean +/− s.e.m.) during the period of stopped flow; inspired water, however, was in acid-base equilibrium (delta pH=−0.002+/−0.01; N=22). The acid-base disequilibrium in expired water was abolished (delta pH=−0.005+/−0.01; N=6) by the addition of bovine carbonic anhydrase (5 mg l-1) to the external medium. Addition of the carbonic anhydrase inhibitor acetazolamide (1 mmol l-1) to the water significantly reduced the magnitude of the pH disequilibrium (from −0.133+/−0.03 to −0.063+/−0.02; N=4). However, after correcting for the increased buffering capacity of the water caused by acetazolamide, the acid-base disequilibrium during stopped flow was unaffected by this treatment (control delta [H+]=99.8+/−22.8 micromol l-1; acetazolamide delta [H+]=81.3+/−21.5 micromol l-1). In rainbow trout, expired water displayed an acid-base disequilibrium (delta pH=0.09+/−0.01; N=6) that also was abolished by the application of external carbonic anhydrase (delta pH=0.02+/−0.01).The origin of the expired water acid-base disequilibrium was investigated further in dogfish. Intravascular injection of acetazolamide (40 mg kg-1) to inhibit internal carbonic anhydrase activity non-specifically and thus CO2 excretion significantly diminished the extent of the expired water disequilibrium pH after 30 min (from −0.123+/−0.01 to −0.065+/−0.01; N=6). Selective inhibition of extracellular carbonic anhydrase activity using a low intravascular dose (1.3 mg kg-1) of the inhibitor benzolamide caused a significant reduction in the acid-base disequilibrium after 5 min (from −0.11+/−0.01 to −0.07+/−0. 01; N=14). These results demonstrate that the expired water acid-base disequilibrium originates, at least in part, from excretory CO2 and that extracellular carbonic anhydrase in dogfish may have a significant role in carbon dioxide excretion. However, externally oriented carbonic anhydrase (if present in dogfish) plays no role in catalysing the hydration of the excretory CO2 in water flowing over the gills and thus is unlikely to facilitate CO2 excretion.

scholarly journals Carbonic anhydrase inhibitors modify intracellular pH transients and contractions of rat middle cerebral arteries during CO2/HCO3– fluctuations

2017 ◽  
Vol 38 (3) ◽  
pp. 492-505 ◽  
Author(s):  
Jacob K Rasmussen ◽  
Ebbe Boedtkjer
Keyword(s):  
Carbonic Anhydrase ◽  
Intracellular Ph ◽  
Cerebral Arteries ◽  
Carbonic Anhydrase Activity ◽  
Carbonic Anhydrases ◽  
Intracellular Acidification ◽  
Acid Base ◽  
Surface Ph ◽  
Middle Cerebral Arteries ◽  
Carbonic Anhydrase Inhibition

The CO2/HCO3– buffer minimizes pH changes in response to acid–base loads, HCO3– provides substrate for Na+,HCO3–-cotransporters and Cl–/HCO3–-exchangers, and H+ and HCO3– modify vasomotor responses during acid–base disturbances. We show here that rat middle cerebral arteries express cytosolic, mitochondrial, extracellular, and secreted carbonic anhydrase isoforms that catalyze equilibration of the CO2/HCO3– buffer. Switching from CO2/HCO3–-free to CO2/HCO3–-containing extracellular solution results in initial intracellular acidification due to hydration of CO2 followed by gradual alkalinization due to cellular HCO3– uptake. Carbonic anhydrase inhibition decelerates the initial acidification and attenuates the associated transient vasoconstriction without affecting intracellular pH or artery tone at steady-state. Na+,HCO3–-cotransport and Na+/H+-exchange activity after NH4+-prepulse-induced intracellular acidification are unaffected by carbonic anhydrase inhibition. Extracellular surface pH transients induced by transmembrane NH3 flux are evident under CO2/HCO3–-free conditions but absent when the buffer capacity and apparent H+ mobility increase in the presence of CO2/HCO3– even after the inhibition of carbonic anhydrases. We conclude that (a) intracellular carbonic anhydrase activity accentuates pH transients and vasoconstriction in response to acute elevations of pCO2, (b) CO2/HCO3– minimizes extracellular surface pH transients without requiring carbonic anhydrase activity, and (c) carbonic anhydrases are not rate limiting for acid–base transport across cell membranes during recovery from intracellular acidification.

1123: Renal Oxalate Transport Depends on Local Carbonic Anhydrase Activity in the Proximal Tubule

2004 ◽  
Vol 171 (4S) ◽  
pp. 296-296
Author(s):  
Michael Straub ◽  
Joséphine Befolo-Elo ◽  
Richard E Hautmann ◽  
Edgar Braendle
Keyword(s):  
Carbonic Anhydrase ◽  
Proximal Tubule ◽  
Carbonic Anhydrase Activity ◽  
Oxalate Transport

RENAL CARBONIC ANHYDRASE IN PREMATURE AND MATURE INFANTS

PEDIATRICS ◽  
1951 ◽  
Vol 7 (2) ◽  
pp. 182-185
Author(s):  
RICHARD DAY ◽  
JANE FRANKLIN
Keyword(s):  
Carbonic Anhydrase ◽  
Premature Infants ◽  
Carbonic Anhydrase Activity ◽  
Renal Carbonic Anhydrase

The carbonic anhydrase activity in the kidneys of premature infants was studied because it was thought that if the renal enzyme is as deficient as that in the blood, inefficiency in acidification of urine might result. In contrast with the blood, postmortem specimens of kidneys of premature infants were found to exhibit carbonic anhydrase activity similar to that found in the case of kidneys from older infants and adults.

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