On the activity of a prostaglandin-dehydrogenase system in the kidney

Nissen, H. Melchior; Andersen, Hans Thor

doi:10.1007/bf00309868

Cited by 20 publications

(6 citation statements)

References 12 publications

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“…15-PGDH expression was minimal in glomerulus, macula densa, and inner medulla/papilla in normal rodent kidney. The localization of 15-PGDH mRNA and protein in the current studies agrees with previous activity studies indi- cating that 15-PGDH activity was high in isolated proximal tubule and in cortical and outer medullary slices but low in inner medulla/papilla (14,19,27). Therefore, 15-PGDH is expressed at the sites in the kidney where COX-2 expression is either not detectable or is only minimally expressed.…”

Section: Discussionsupporting

confidence: 91%

“…15-PGDH oxidizes the 15(S)-hydroxyl group of prostaglandins to yield inactive 15-keto metabolites (8,16). Previous reports have shown that 15-PGDH activity is higher in kidney cortex (particularly in the proximal tubule) and outer medulla than in inner medulla/ papilla (14,19,27). Kidney 15-PGDH activity has been reported to be increased in obstructive kidneys (10) but inhibited by estradiol (5).…”

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confidence: 99%

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Renal localization and regulation of 15-hydroxyprostaglandin dehydrogenase

Yao¹,

Xu²,

Harris³

et al. 2008

American Journal of Physiology-Renal Physiology

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Tissue prostaglandin levels are determined by both biosynthesis and catabolism. The current studies report the expression and localization of 15-hydroxyprostaglandin dehydrogenase (15-PGDH), a key enzyme in prostaglandin catabolism in the kidneys. We also investigated potential interactions between 15-PGDH and cyclooxygenase (COX), a key enzyme in prostaglandin biosynthesis. Both 15-PGDH mRNA and protein levels were significantly higher in kidney cortex than in papilla, which is opposite to the expression pattern of COX-2. In situ hybridization indicated that 15-PGDH mRNA was mainly localized to the tubular epithelial cells in kidney cortex and outer medulla but not in the glomerulus or papilla. Dual immunofluorescent staining indicated that 15-PGDH was expressed in the proximal tubule, cortical, and outer medullary thick ascending limb and collecting duct but not in the macula densa or papilla. 15-PGDH levels were significantly lower in a macula densa cell line (MMDD1) than in a proximal tubule cell line. Although a high-salt diet decreased COX-2 expression in macula densa, it increased macula densa 15-PGDH expression in both mouse and rat kidneys. In MMDD1 cells, a COX-2 inhibitor increased 15-PGDH, whereas a COX-1 inhibitor had no effect. Furthermore, intense 15-PGDH immunofluorescent staining was found in both macula densa and glomerulus in COX-2 knockout mice. The intrarenal distribution of 15-PGDH and its interactions with COX-2 suggest that differential regulation of COX-2 and 15-PGDH may play an important role in determining levels of prostaglandins involved in regulation of salt, volume, and blood pressure homeostasis. kidney; prostaglandin catabolism; cyclooxygenase; macula densa IN ADULT MAMMALIAN KIDNEY, prostaglandins regulate renal hemodynamics and salt and water homeostasis (11). Prostaglandin production depends on the release of arachidonic acid from membrane phospholipids by specific phospholipases and subsequent conversion to prostaglandin H 2 (PGH 2 ) by cyclooxygenase (COX

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Section: Discussionsupporting

confidence: 91%

mentioning

confidence: 99%

Renal localization and regulation of 15-hydroxyprostaglandin dehydrogenase

Yao¹,

Xu²,

Harris³

et al. 2008

American Journal of Physiology-Renal Physiology

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“…Using both high-pressure liquid chromatography and TLC techniques these workers demonstrated a lack of conversion of prostaglandin E to prostaglandin F, and the presence of two major metabolite peaks one (possibly 15-keto-PGE2) with an Rf very close to that of PGE2. Histochemical evidence indicates that the loop of Henle is the major segment of the nephron which contains the prostaglandin-metabolizing enzyme, prostaglandin-15-OH dehydrogenase (Nissen & Anderson, 1968). In addition, the microinjection experiments of Cagen & Kauker (1983) (Kauker, 1975;Cagen & Kauker, 1983;Haylor & Towers, 1987).…”

Section: Discussionmentioning

confidence: 99%

Tubular mechanisms determining the urinary excretion of tritiated prostaglandin E2 in the anaesthetized rat.

Haylor

Lote

Towers

1988

The Journal of Physiology

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“…The PGE, appearing intact in the urine is considered to be of renal origin, 14 entering the tubular fluid of the loop of Henle. 16 Oxidation to 15-keto metabolites may occur during passage of the tubular fluid through the more distal portions of the nephron; in the rat kidney, PGDH activity appears predominantly in the thick ascending limb of the loop of Henle. "…”

Section: Discussionmentioning

confidence: 99%

Renal prostaglandin excretion and metabolism in male and female New Zealand normotensive and genetically hypertensive rats.

Baer¹,

Cagen²

1981

Hypertension

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SUMMARY Reduced renal 15-hydroxyprostaglandin dehydrogenase (PGDH) activity has been proposed as a cause, subsequent to elevation of intrarenal prostaglandin (PG) E, levels, of the development or maintenance of high blood pressure (BP) in the New Zealand genetically hypertensive (NZGH) rat. To test this hypothesis, PGDH activity in homogenates of kidneys and lungs and in urine concentration and excretion of PGE, were determined in male and female NZGH and normotensive control (NZNR) rats. Lung PGDH activities of the four groups were similar. Renal PGDH activity was 50% lower for the male NZGH than for the male NZNR, but for the female rats no difference in renal PGDH activity was found between NZGH and NZNR. In addition, there was a large sex-related difference in renal PGDH activities, values for the female rats being only 5% to 10% of the values for males. Urine PGE, concentration and excretion were two to five times greater for the female rats than for the males, but did not differ between male NZGH and male NZNR. From these observations, it appears that neither renal PGDH activity nor urine PGE, levels is associated with hypertension in the New Zealand genetically hypertensive strain of rats. 1 Although the causal mechanism underlying the development of high blood pressure (BP) in this strain remains undefined, it has been proposed that altered prostaglandin (PG) metabolism in the kidney may be a contributing factor. The basis for this proposal rests on several observations. Armstrong et al. 3 found that the activity of 15-hydroxyprostaglandin dehydrogenase (PGDH) in kidneys from male NZGH is only about 30% of that in kidneys from male NZNR, but that renal prostaglandin (PG) synthetase activities were not different. PGDH is a major prostaglandincatabolizing enzyme in rat kidney, oxidizing PGEj and PGF,a to 15-keto metabolites,' and its activity could be a determinant of intrarenal levels of these 1 From these observations, it was proposed that increased PGE, levels in the kidney, resulting from lower PGDH activity, might contribute to the development or maintenance of hypertension in the NZGH, through direct or indirect renal vasoconstrictor effects of PGE,. 2We recently observed, in normal Wistar rats, that PGDH activity is approximately 40 times greater in the kidneys of males than in the kidneys of females; 7 this difference between male and female normotensive rats is far greater than the differences reported 1 ' *~1 0 between genetically hypertensive and normotensive male rats. In the present study, we have compared renal prostaglandin metabolizing activity, and urinary prostaglandin excretion, in male and female rats of the New Zealand genetically normotensive and hypertensive strains. In addition to confirming that PGDH activity is lower in the kidneys of male NZGH than in the kidneys of male NZNR, we found that renal PGDH activity of female NZGH and NZNR is much lower than that of the males of the two strains. In addition, we found no difference between the PGDH activities of female NZGH and female N...

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On the activity of a prostaglandin-dehydrogenase system in the kidney

Cited by 20 publications

References 12 publications

Renal localization and regulation of 15-hydroxyprostaglandin dehydrogenase

Renal localization and regulation of 15-hydroxyprostaglandin dehydrogenase

Tubular mechanisms determining the urinary excretion of tritiated prostaglandin E2 in the anaesthetized rat.

Renal prostaglandin excretion and metabolism in male and female New Zealand normotensive and genetically hypertensive rats.

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