Experiments were conducted on 119 male and female mongrel/albino rats and on 5 male rabbits to study the mechanisms of the in vivo effect of the inhibitors of the biosynthesis of prostaglandins, acetylsalicylic acid, and indometacin, taking into account the previously obtained data on the fact that these inhibitors elevate mean arterial pressure and increase vasopressor sensitivity to adrenalin and noradrenaline in experimental animals. It was found that these inhibitors of prostaglandin biosynthesis promote the development of "salt hypertension" in rats against the background of a noticeable increase in vasopressor sensitivity to catecholamines. Intravenous administration to rabbits of angiotensin-11 in pressor doses causes an increase in the content of group E prostaglandins in the blood plasma of rabbits and a decrease in the renin activity ("feedback" effect). The data obtained have confirmed the assumption that prostaglandins take part in the arterial pressure control and suggested that in exhaustion or hereditary deficiency of the function of the prostaglandin production system the vessels may escape the depressor control, in this case the sensitivity to pressor factors increase and stable arterial hypertension develops.