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Query: UNIPROT:P41181 (collecting duct)
 5,183 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thirty minutes after indomethacin (10 mg/kg, iv), a prostaglandin synthesis inhibitor, had been given to 10 rats, the Na concentration in renal papilla averaged 349 mEq/kg H2O, whereas it averaged only 181 in 14 "non-indomethacin" control rats (P less than 0.0001). Papillary plasma flow was closely similar in both groups. In a subsequent study, eight "indomethacin" rats had the same papillary flow as seven non-indomethacin rats but had a papillary Na concentration of 358 vs. 185 in the non-indomethacin controls (P less than 0.0001). In nine more rats, indomethacin increased Cl concentration in papillas by 66% (P less than 0.0001), while Na concentration increased 60% (P less than 0.0001). In eight other rats, micropuncture indicated that indomethacin does not greatly alter delivery of fluid out of late proximal tubule. Meclofenamate, another inhibitor, increased papillary Na just as much as indomethacin. Papillary urea is not changed with indomethacin. Thus, papillary Na concentration was almost twice as high in indomethacin rats, despite similar papillary plasma flow and late proximal flow. Apparently, inhibiting prostaglandin synthesis is associated with either a great increase in Na or Cl "pumping" or a great decrease in Na or Cl "leak" in either collecting duct or ascending limb, or in both. The collecting duct and papillary interstitial cells both synthesize prostaglandins, which seem to have a profound effect on medullary net Na transport.
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PMID:Evidence that prostaglandin synthesis inhibitors increase the concentration of sodium and chloride in rat renal medulla. 87 Feb 22

The role of prostaglandins in the regulation of sodium and water excretion has been widely studied, but little is known about the influence of prostaglandins (PGs) on the tubular handling of calcium, magnesium or phosphorus. Recent observations have suggested that PGE2 and vasopressin may interact and influence reabsorption of calcium and phosphorus in the cortical collecting duct. The present study investigated the effect of meclofenamate (2 mg/kg), and inhibitor of PG synthesis, on the excretion of calcium, magnesium and phosphorus. Experiments were performed in antidiuretic and water diuretic rats to examine potential PG-vasopressin interactions on the reabsorption of these ions by renal tubules. In antidiuretic rats given meclofenamate, urine osmolality increased whereas urine flow and the fractional excretion of water, urea, sodium, calcium and magnesium decreased by 30 to 50%. In water diuretic animals, urine osmolality and urea excretion were unaltered after meclofenamate administration. Fractional excretion of sodium, water, calcium and magnesium declined approximately 50% in water diuretic rats given meclofenamate. Urinary excretion of PGE2 was not significantly different in water diuretic and antidiuretic rats averaging 262 +/- 78 vs. 167 +/- 35 pg/min, respectively. Meclofenamate significantly reduced urinary excretion of PGE2 in both groups. The results indicate that renal PGs modulate renal tubular reabsorption of calcium and magnesium, as well as sodium and water.
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PMID:Prostaglandin-vasopressin interactions on the renal handling of calcium and magnesium. 658 91

The present study examines the possibility that prostaglandins affect the renal tubular handling of urea. Meclofenamate (1 mg.kg-1.h-1), an inhibitor of prostaglandin synthesis, decreased fractional urea clearance from 86 to 67%, increased urine osmolality, and decreased the fractional excretion of water in rats undergoing a hypertonic sodium chloride diuresis. The percentage of [14C]urea microinjected into distal convoluted tubules that was recovered in urine fell from 75 to 64% (P less than 0.01) after meclofenamate. The fraction of injected urea excreted like inulin (direct recovery) was reduced from 20 to 8% (P less than 0.0001) by meclofenamate. Addition of PGE2 (1.2 or 89 pmol) or PGF2 alpha (1.4 pmol) to the microinjectate returned the urinary recovery of the microinjected [14C]urea to the control level, but PGA2 (3 pmol) did not. Direct urea recovery was doubled by PGE2 or PGF2 alpha. These results indicate that prostaglandin E2 and F2 alpha inhibit the reabsorption of urea in the collecting duct. Prostaglandins may participate in the renal concentrating mechanism by altering the inner medullary influx of urea.
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PMID:Prostaglandin E2 and F2 alpha reduces urea reabsorption from the rat collecting duct. 724 74