Spontaneous changes in isometric developed tension (IDT) as a function of time after isolation (contractile constancy) in uteri from control-castrated and castrated chronic streptozotocin-diabetic rats, were explored. The effects of injecting 17-beta estradiol (E 0) were also studied. No differences in the minor changes of contractile constancy, between control and diabetic preparations, during a period of 60 min, were detected, whereas uteri from non-diabetic E O injected animals (0.5+1.0 ug, prior to sacrifice), exhibited a profound reduction of IDT, significantly greater than in tissues obtained from E 0 injected-diabetic rats. Moreover, basal generation and outputs into the suspending solution of prostaglandins (PGs) E 1, E 2 and F 2α, were explored in the same groups, at 60 min following tissue isolation. The basal outputs of these three PGs were similar in castrated control rats, but preparations from castrated-diabetics released significantly more PGE 1. The administration of E 0 to castrated-diabetics, failed to alter the releases of the three PGs explored. In addition, the metabolism of labelled arachidonic acid (AA) into different prostanoids (6-keto-PGF 1, PGF 2, PGE 2 and thromboxane B 2-TXB 2), was also investigated. The non-diabetic spayed rat uterus converted AA into these four prostanoids, the transformation into 6-keto-PGF 1α (as an index of PGI 2 formation) being the most prominent. In preparations from diabetic rats the formation) being the most prominent. In preparations from diabetic rats the formation of 6-keto-PGF 1α, PGF 2α and PGE 2, was significantly smaller than in controls, whereas a greater % of TXB 2 formation (as an index of TXA 2), was detected. On the other hand uterine preparations from non-diabetic spayed rats injected with E 0 formed less 6- keto-PGF 1α and PGE 2 and similar amounts of PGF 2α or of TXB 2 from AA, than E 0 injected controls, whereas uteri from castrated diabetic animals injected with E 0, formed a similar % of 6-keto-PGF 1α, PGF 2α and PGE 2 from AA, than tissue preparations from non-estrogenized controls. However, the enhanced transformation of the labelled fatty acid precursor (AA) into TXB 2 in the diabetic group, was significantly reduced by the steroid. The role of the augmented generation and release of PGE 1 in uteri from diabetic rats is discussed in terms of precedents indicating the relevance of PGs type E supporting rat uterine motility. In addition the influence of E 0 is attractive, because its reducing effect on TX production, in diabetes, a disease known to be accompanied by enhanced synthesis of vasoconstrictor and platelet aggregation TXA 2, and by frequent obstructive circulatory problems.