Deleterious action of vasopressin in gastroduodenal ulceration: experimental and clinical observations

Vasopressin, released from the posterior pituitary and from the vascular endothelium, can cause vasoconstriction and provoke platelet aggregation, leading to an impaired tissue blood supply. In humans with pituitary diabetes insipidus the central release of vasopressin is diminished, and in the Brattleboro homozygous rat there is congenitally no synthesis of this hormone. The gastroduodenal intramucosal vasopressin level is elevated in normal rats following various acute ulcerogenic challenges (after ethanol, reserpine, indomethacin, cold-restraint stress, endotoxin shock and hemorrhagic shock), and vasopressin-deficient rats are less sensitive to these stimuli. In a hospital- and population-based case-control, age-matched retrospective study, the incidence of human gastroduodenal ulceration is significantly higher in the normal population (in whom the release of vasopressin is presumed to be intact) than in the vasopressin-deficient one (central diabetes insipidus patients). In conclusion, endogenous vasopressin plays an aggressive role in development of gastroduodenal ulceration, especially that related to stress.