Marcela Coltau

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The aim of the present study was to follow the effect of nitric oxide (NO) on carbonic anhydrase in vitro and in vivo. The effect of L-arginine (as source of NO), as well as that of its analogue, nitro-G-monomethyl-L-arginine, an inhibitor of NO synthesis on carbonic anhydrase, were also studied. In vitro results showed that L-arginine activates carbonic(More)
Previous studies by this research team proved that vasodilating prostaglandins (PGs) E1, E2 and I2 inhibit carbonic anhydrase (CA) in vitro and in vivo, which suggested involvement of CA in gastric acid secretion inhibition and the increase of gastric mucosa blood flow produced by this group of PGs. Relying on these findings, as well as on our clinical(More)
In this study our experiments followed in vitro and in vivo the effect of omeprazole on purified and erythrocyte carbonic anhydrase (CA) I and II isozymes, as well as on gastric mucosa CA IV in humans. Our in vitro results show that omeprazole-induced inhibition of purified CA I and CA II and gastric mucosa CA IV is dose- and pH-dependent. In vivo, the i.v.(More)
1. At present, CO2 is considered to be the most important factor in regulating cerebral blood flow by modification of the interstitial fluid and extracellular pH, but the mechanism by which hypercapnia produces vasodilation is still controversial. In the present paper we investigated the effect of hypercapnia on carbonic anhydrase (CA) activity. We also(More)
Five years ago, our in vitro and in vivo studies demonstrated for the first time that diuretic agents such as furosemide, hydrochlorothiazide, amiloride, triamterene and spironolactone inhibit carbonic anhydrase (CA) I, II and renal CA IV by a direct mechanism of action. In this paper we investigate the relationship between diuretics and CA I in the(More)
Previous work carried out by our team in vitro regarding the relationship between prostaglandins (PGs) and carbonic anhydrase (CA) has shown that prostaglandins E1 (PGE1), E2 (PGE2) and I2 (PGI2) inhibit purified bovine red cell CA, as well as human red cell and gastric mucosa CA. This is a completion of our previous research work including kinetic and in(More)
Previous data concerning the action of calcium (Ca) on gastric acid secretion (GAS) indicated that calcium ions increase GAS elicited by gastrin released through a vagal mechanism, and also by a direct effect on parietal cells. Our research showed that the stimulating effect of calcium on gastric acid secretion can be antagonized by verapamil(More)
This study assessed the efficacy of ebrotidine (N-[(E)-[[2-[[[2-[(diaminomethylene)amino]-4-thiazolyl] methyl]thio]ethyl]amino]methylene]-4-bromo-benzenesulfonamide, CAS 100981-43-9, FI-3542) versus ranitidine and placebo in preventing gastroduodenal lesions induced by piroxicam. Thirty patients with rheumatic disease, who were divided into 5 groups,(More)
In this article we studied in vitro and in vivo the effect of calcium channel blockers (verapamil and amlodipine) on erythrocyte carbonic anhydrase I activity, on carbonic anhydrase I isolated from vascular smooth muscles, and on arterial blood pressure values in human beings and in animals. Our in vitro and in vivo results have shown that verapamil and(More)
OBJECTIVES In this paper we investigated the effect of indomethacin, acetazolamide and their combination in vitro and in vivo on carbonic anhydrase (CA) isozymes. METHOD In vitro experiments followed the effect of the two substances at concentrations between 10(-8)-10(-4) M on purified human red cell CA I and II as well as on human gastric mucosa CA IV(More)