scholarly journals Carbonic anhydrase inhibition ameliorates Aβ‐induced neurovascular dysfunction in vivo

2020 ◽  
Vol 16 (S3) ◽  
Author(s):  
Elisa Canepa ◽  
Rafael Vazquez‐Torres ◽  
Ludovic Debure ◽  
Silvia Fossati
2021 ◽  
Vol 36 (1) ◽  
pp. 964-976
Author(s):  
Ilaria Dettori ◽  
Irene Fusco ◽  
Irene Bulli ◽  
Lisa Gaviano ◽  
Elisabetta Coppi ◽  
...  

Nature ◽  
1952 ◽  
Vol 170 (4325) ◽  
pp. 499-499 ◽  
Author(s):  
HENRY D. JANOWITZ ◽  
HENRY COLCHER ◽  
FRANKLIN HOLLANDER

2015 ◽  
Vol 31 (6) ◽  
pp. 894-899 ◽  
Author(s):  
Lorenzo Di Cesare Mannelli ◽  
Laura Micheli ◽  
Fabrizio Carta ◽  
Andrea Cozzi ◽  
Carla Ghelardini ◽  
...  

1977 ◽  
Vol 43 (4) ◽  
pp. 582-590 ◽  
Author(s):  
E. D. Crandall ◽  
A. Bidani ◽  
R. E. Forster

A rapidly responding stopped-flow glass pH electrode apparatus was used to investigate pH changes in blood in vivo after it exits from an exchange capillary. Arterial blood was drawn from anesthetized animals through the apparatus. Temperature and pH of the blood in the electrode chamber were continuously recorded, both during withdrawal and after flow was stopped. Blood pH did not change after stopping flow in control experiments. When benzolamide (2 mg/kg) was given to inhibit carbonic anhydrase activity available to plasma (e.g., due to lysis) while having less effect on intracellular activity, pH increased 0.02–0.04 (t1/2 approximately 8 s) after stopping flow. Administration of acetazolamide (50 mg/kg) resulted in pH decreasing 0.07–0.10 (t1/2 approximately 15 s) after stopping flow. Ventilation for 1 min with N2 resulted in an increased rise in pH for the benzolamide-treated animals but a decreased fall in pH for the acetazolamide-treated animals. These shifts in arterial blood pH after gas exchange are largely due to disequilibrium of [H+] between red cells and plasma at the end of the pulmonary capillary.


1976 ◽  
Vol 230 (6) ◽  
pp. 1517-1523 ◽  
Author(s):  
MH Humphreys

The effect of furosemide on intestinal absorption of water and electrolytes was studied using segments of rat ileum perfused in vivo. Furosemide (1 mM) in the perfusion fluid reduced absorption of Na, Cl, and water by 50% from a balanced electrolyte solution without changing the transepithelial potential difference (PD). This effect was also observed in the absence of luminal glucose and was largely reversible. Substitution of all Na in perfusion fluid with choline produced secretion of Na and water and abolished Cl absorption; substitution of all Cl with SO4 reduced Na absorption to 20% of control values. Under both these conditions, furosemide had only trivial effects on electrolyte absorption and exerted no effect on PD. Measurements of unidirectional fluxes of Na and Cl showed that furosemide decreased net flux by reducing lumen-to-blood flux of these ions rather than increasing blood-to lumen flux. These results resemble those obtained in this tissue following exposure to acetazolamide, and suggest that furosemide inhibits a coupled, neutral process of NaCl transport from lumen to blood. Although this effect could be a result of carbonic anhydrase inhibition it more likely occurs from a separate action of furosemide on ileal transport.


1979 ◽  
Vol 236 (1) ◽  
pp. F58-F65 ◽  
Author(s):  
M. S. Lucci ◽  
D. G. Warnock ◽  
F. C. Rector

The extent to which bicarbonate reabsorption in the rat proximal convoluted tubule depends on carbonic anhydrase has been examined by in vivo microperfusion and the measurement of total CO2 concentration by microcalorimetry. Tubules were perfused with an ultrafiltrate-like solution at 13 nl/min, and volume reabsorptive rate (JV) was measured using [14C]inulin. Addition of either 800 or 100 microM acetazolamide to the perfusion solution completely inhibited the reabsorption of total CO2. The control total CO2 reabsorptive rate (JtCO2) was 147 +/- 23 pmol/mm.min, and acetazolamide reduced JtCO2 to -3 +/- 5 pmol/mm.min. Acetazolamide reduced JV by 65% from a control of 2.3 +/- 0.4 to 0.8 +/- 0.1 nl/mm.min. The dose-response curve for acetazolamide showed that the I50 for inhibition of JtCO2 was 4 microM. The inactive congener of acetazolamide, t-butyl acetazolamide, did not reduce JV or inhibit bicarbonate reabsorption, indicating that the effect of acetazolamide on JtCO2 was specific for carbonic anhydrase inhibition. Since bicarbonate reabsorption was completely blocked by carbonic anhydrase inhibition, there is no need to postulate either carbonic acid recycling or carbonic anhydrase-independent bicarbonate reabsorption.


1972 ◽  
Vol 16 (3) ◽  
pp. 377-385 ◽  
Author(s):  
D.T. Zborowska-Sluis ◽  
D.P. Tozzi ◽  
G.A. Klassen

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