Introdution. Several investigations have shown that the renal medulla has a grater capacity to generate cyclooxygenase than the renal cortex. To further evaluate the change of cyclooxygenase synthesis in the kidney, particularly in the outer medulla, in disorders involving fluid and electrolyte imbalances, we sought to determine renal cyclooxygenase expression in the diabetic rates. Methods. We determined renal cyclooxygenase mRNA and urinary prostaglandin E2 and thromboxame B2 excretion in 10 normal and 10 streptozotocin-induced diabetic rats by reverse transcription-polymerase chain reaction and with enzyme immunoassay, respectively. Cyclooxygenase immunoreactivity was detected by immunohistochemistry in for normal and four diabetic rats. Results. Cyclooxygenase 1 mRNA were 1.4-fold and 2.8-fold increased in the cortex and outer medulla, and Cyclooxygenase 2 mRNA was 2.6-fold increased in the outer medulla of 10 diabetic rats, as compared with 10 normal rats. Urinary prostaglandin E2 and thromboxane B2 excretion rate were significantly increased from 6 and 2 weeks after diabetic induction. In normal rats, immunohistochemical studies showed positive cyclooxygenase 1 and cyclooxygenase 2 immunostaining in almost all segments of renal tubules. Diabetic rats had the greatest enhancement of immunostaining for cyclooxygenase 1 in the proximal straight tubule, cortical collecting tubule and medullary collecting tubule, and for cyclooxygenase 2 in the proximal straight tubule and medullary thick ascending limb. Conclusion. Our results indicate that increases in cyclooxygenase 1 and cyclooxygenase 2 synthesis in the kidney, particularly in the outer medulla, possibly play an important part in the adaption of renal function to hyperglycemian and hyperosmolarity in diabests.