Prostaglandins with vasodilating effects inhibit carbonic anhydrase while vasoconstrictive prostaglandins and leukotriens B4 and C4 increase CA activity.

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 vivo studies concerning the relationship between PGs and CA. The relationship between CA and PGE1, E2 and I2, known for their vasodilating and gastric acid secretion (GAS) reducing effects, on the one hand, and between CA and prostaglandin F2 alpha (PGF2 alpha), thromboxans A2 (TXA2), and B4, C4 leukotriens (LTB4, LTC4), known for their vasoconstrictive effects, on the other hand, were studied in vitro. The in vivo studies followed changes induced by vasodilating PGs (misoprostol-analogue of PGE1, nalador-analogue of PGE2, ilomedin-analogue of PGI2) and vasoconstrictive-minprostin analogue of PGF2 alpha on red cell CA, correlated to modifications of arterial blood pressure (BP). Results obtained in vitro show that PGE1, E2, I2 inhibits basal CA activity, while PGF2 alpha, TXA2 and LTB4, LTC4 increase the activity of the enzyme. Kinetic assessments show that the inhibition and the activation mechanism is a direct one of the non-competitive type located on the active site of CA. Data obtained in vivo show that administration of a single therapeutic dose of misoprostol, nalador or ilomedin inhibits basal activity of CA by 35-55% with corresponding decrease of BP values.(ABSTRACT TRUNCATED AT 250 WORDS)