Effect of synthesis inhibitors of thromboxane A2 and prostaglandin E2 on the regulation of sodium and water.

The aim of this study was to evaluate the response to water deprivation in rats during development in the presence and in the absence of either benzylimidazole or acetaminophen (10 mg/kg of each), inhibitors of the synthesis of thromboxanes and other arachidonic acid metabolites. Whereas water deprivation induced an increment in urine osmolality both in control and vehicle-treated animals, this response was blocked by benzylimidazole and acetaminophen in the 5-day-old rats. No effect was observed in the older rats. Benzylimidazole also increased sodium excretion in the newborn rat. To assess the effect of benzylimidazole on epithelial cells deprived of the influence of hemodynamic factors, sodium transport and water flow were studied in the frog skin and in the toad bladder, respectively. In the frog skin epithelium, benzylimidazole (10(-4) M) inhibited the vasopressin-stimulated (100 mU/ml) sodium transport and in the toad bladder it decreased the vasopressin-stimulated (5 mU/ml) hydroosmotic flow. Our results suggest that thromboxanes are necessary for a full development of the response to vasopressin in sensitive epithelia. In the rat, thromboxanes and other arachidonic acid metabolites appear to play a role in the neonate but not in the older animal.