Indomethacin activates carbonic anhydrase and antagonizes the effect of the specific carbonic anhydrase inhibitor acetazolamide, by a direct mechanism of action

International Journal of Clinical Pharmacology and Therapeutics

Volumn 39, Issue 6, 2001, Pages 265-270

  Puscas, I ^a   Ifrim, M ^a   Maghiar, T ^a   Coltau, M ^a   Domuta, G ^a   Baican, M ^a   Hecht, A ^a  

^a Ctr for Res and Medical Assistance   (Romania)

Author keywords

Acetazolamide; Carbonic anhydrase isozymes; Gastric acid secretion; Indomethacin

Indexed keywords

ACETAZOLAMIDE; CARBONATE DEHYDRATASE; CARBONATE DEHYDRATASE II; CARBONATE DEHYDRATASE INHIBITOR; CARBONATE DEHYDRATASE IV; INDOMETACIN; ISOENZYME; PROSTAGLANDIN; PROSTAGLANDIN SYNTHASE INHIBITOR; UNCLASSIFIED DRUG;

ACID BASE BALANCE; ARTICLE; CLINICAL TRIAL; CONCENTRATION RESPONSE; CONTROLLED CLINICAL TRIAL; CONTROLLED STUDY; CORRELATION FUNCTION; DOSE RESPONSE; DRUG MECHANISM; ENZYME ACTIVATION; ENZYME ACTIVITY; ENZYME INHIBITION; ENZYME PURIFICATION; ERYTHROCYTE; HUMAN; HUMAN EXPERIMENT; HYPOTHESIS; IN VITRO STUDY; IN VIVO STUDY; NORMAL HUMAN; PH; PHARMACOKINETICS; PROSTAGLANDIN SYNTHESIS; STOMACH MUCOSA; STOMACH SECRETION;

ACETAZOLAMIDE; ANTI-INFLAMMATORY AGENTS, NON-STEROIDAL; CARBONIC ANHYDRASE INHIBITORS; CARBONIC ANHYDRASES; DOSE-RESPONSE RELATIONSHIP, DRUG; DRUG INTERACTIONS; ENZYME ACTIVATION; GASTRIC MUCOSA; HUMANS; INDOMETHACIN;

EID: 0034991958     PISSN: 09461965     EISSN: None     Source Type: Journal    
DOI: None     Document Type: Article

References (30)

1. 2 on reduction of gastric mucosal blood flow caused by indomethacin in rats
2. Renal syndromes associated with non-steroidal anti-inflammatory drugs
3. Gastric carbonic anhydrase
4. Indomethacin damage to rat gastric mucosa is markedly dependent on luminal pH
5. Non-steroidal anti-inflammatory drugs and peptic ulcers
6. The carbon dioxide hydration activity of carbonic anhydrase: Stop-flow kinetic studies on the native human isozymes B and C
7. Gastric cytoprotection by acetazolamide. Role of endogenous prostaglandins
8. The effects of anti-ulcer agents on indomethacin-induced gastric ulceration in the rat
9. Inhibitory effect of non-steroidal anti-inflammatory drugs on mucosal cell proliferation associated with gastric ulcer healing
10. Amount and distribution of carbonic anhydrases CA I and CA II in the gastrointestinal tract
11. Carbonic anhydrase: Chemistry, physiology and inhibition
12. Carbonic anhydrase: The middle years 1945-1960, and introduction to pharmacology of sulfonamides
13. Chemical properties of carbonic anhydrase IV, the membrane-bound enzyme
14. Carbonic anhydrase: Its preparation and properties
15. Inhibitory effect of indomethacin on prostacyclin receptor-mediated cerebral vascular responses
16. Carbonic anhydrase inhibitors in the treatment of gastric and duodenal ulcers
17. Farmacologia clinica do aparelho digestivo
18. Inhibition of carbonic anhydrase by nitric oxide
19. 4 increase CA activity
20. Non-steroidal anti-inflammatory drugs activate carbonic anhydrase by a direct mechanism of action
21. Isosorbide nitrates, nitroglycerin and sodium nitroprusside induce vasodilation concomitantly with inhibition of carbonic anhydrase I in erythrocytes
22. Carbonic anhydrase is a modulator of vasculary and secretory processes in the organism. The pH theory
23. Vasodilatory effect of diuretics is dependent on inhibition of vascular smooth muscle carbonic anhydrase by a direct mechanism of action
24. A new concept regarding the mechanism of action of omeprazole
25. Rapid method for differentiation of carbonic anhydrase I from carbonic anhydrase II activity
26. Ulcer formation and cytoprotection by acetazolamide
27. Duodenal ulcers induced by indomethacin plus histamine in the dog. Involvement of the impaired duodenal alcaline secretion in this pathogenesis
28. Inhibition of prostaglandin synthesis as a mechanism of action for aspirin-like drugs
29. Non-steroidal anti-inflammatory drugs and gastroenteropathy: The second hundred years
30. Indomethacin abolishes cerebral blood flow increase in response to acetazolamide-induced extracellular acidosis: A mechanism for its effect on hypercapnia?