Deficiency in 15-hydroxyprostaglandin dehydrogenase activity after unilateral ureteral obstruction of the dog kidney.
In the present study, metabolism of prostaglandins (PGs) by 15-hydroxyprostaglandin dehydrogenase (15-OH PGDH) was investigated in dog kidneys with ureteral obstruction. After 24 hr of ureteral obstruction, the obstructed kidney and the contralateral kidney were removed and the cytosolic fractions (105,000 X g), enriched in 15-OH PGDH, were prepared from the cortex and medulla. 15-OH PGDH activity was estimated by radiometric assays of the metabolism of [3H]PGE2 and [3H]prostacyclin. Cortical 15-OH PGDH activity decreased by greater than 50% in the ureter-obstructed kidney as compared to the contralateral kidney. Similar results were obtained by estimating the stereo-specific release of tritium from position 15 using 15-[3H]PGF2 alpha as substrate. In contrast to the cortex, there were no differences in 15-OH PGDH activity found in the medulla of the obstructed and contralateral kidneys. Because the cortex contains higher levels of 15-OH PGDH activity, the deficiency in that site may contribute to the elevated levels of PGs in renal venous blood during ureteral obstruction.
D000818:Animals; D015237:Dinoprost; D015232:Dinoprostone; D004285:Dogs; D011464:Epoprostenol / Q000378:metabolism; D006911:Hydroxyprostaglandin Dehydrogenases / Q000172:deficiency* / Q000378:metabolism; D007668:Kidney / Q000201:enzymology*; D009243:NAD / Q000378:metabolism; D011458:Prostaglandins E / Q000378:metabolism; D011460:Prostaglandins F / Q000378:metabolism; D012079:Renal Circulation; D013237:Stereoisomerism; D013379:Substrate Specificity; D014517:Ureteral Obstruction / Q000201:enzymology*
D011458:Prostaglandins E; D011460:Prostaglandins F; D009243:NAD; D015237:Dinoprost; D011464:Epoprostenol; D006911:Hydroxyprostaglandin Dehydrogenases; C035859:15-hydroxyprostaglandin dehydrogenase; D015232:Dinoprostone