Altered aortic and cremaster muscle prostaglandin synthesis in diabetic rats.

Alterations in the synthesis and release of prostaglandins have been reported in humans and animal models of diabetes mellitus. In the present study synthesis and release of prostaglandins by thoracic aorta and cremaster muscle of rats with streptozotocin-induced diabetes of 8 wk duration was compared with age-matched controls. Prostaglandin synthesis was assessed by the measurement of immunoreactive prostaglandin E2 (PGE2) and 6-ketoprostaglandin F1 alpha (6-keto-PGF1 alpha) release and by quantifying metabolism of exogenous [1-14C]arachidonic acid by thoracic aortic rings and minced cremaster muscle. The cremaster muscles from diabetic rats released significantly greater quantities of PGE2 and 6-keto-PGF1 alpha and PGE2. In contrast, the aortas from diabetic rats released smaller quantities of 6-keto-PGF1 alpha and PGE2 and exhibited reduced 6-[1-14C]keto-PGF1 alpha. These studies indicate that diminished prostacyclin (PGI2) and/or PGE2 production is not a general feature of all diabetic vascular tissues, suggesting that large and small blood vessels may not be similarly affected by diabetes in regard to the metabolism of exogenous arachidonic acid and the synthesis and release of prostaglandins. Furthermore, the vascular changes often observed in conjunction with diabetes, i.e., alterations in vascular reactivity and microangiopathy in small blood vessels and atherosclerosis of large blood vessels may be related in some way to the segmental differences observed in prostaglandin synthesis.