Interaction of Conventional and Antikaliuretic Diuretics with the Renal Prostaglandin System

Kramer, Herbert J.; Düsing, Rainer; Stinnesbeck, B.; Prior, W.; Bäcker, Angela; Eden, J. van; Kipnowski, J.; Glänzer, K; Krück, F.

doi:10.1042/cs0590067

Cited by 39 publications

(7 citation statements)

References 4 publications

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“…Despite this suppression of renal PG biosynthesis [37], however, none of the furosemide-induced changes in renal function were signi ficantly altered during combined treatment with furosemide and indomethacin. This finding strongly contrasts with previous studies demonstrating a blunted natriuretic response to furosemide during pharmaco logical inhibition of PG synthesis [5, [17][18][19], The reason for this discrepancy remains speculative. However, the present data indi cate that the acute tubular effects of large doses of furosemide do not require an intact PG system and consequently are not me diated by PG.…”

Section: Urinary Pge2 Excretioncontrasting

confidence: 55%

“…Its action has been suggested to be mediated -at least in part -by PG since some investigators have found an increase in urinary PG excretion during furosemide treatment [13][14][15][16][17] and its natriuretic effect may be blunted during concomitant inhibi tion of PG biosynthesis [5, [17][18][19], There fore, in the present study, the effects of furo semide on GFR and tubular NaCl absorp tion were studied without and with con comitant administration of indomethacin. Our results support the concept that PG par ticipate in the regulation of chloride absorp tion in the diluting segments of the nephron.…”

Section: Introductionmentioning

confidence: 99%

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Prostaglandins Participate in the Regulation of NaCl Absorption in the Diluting Segments of the Nephron in vivo: Effects of Furosemide

Düsing¹,

Nicolas²,

Glänzer³

et al. 1982

Kidney Blood Press Res

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Various studies point to a role of the renal prostaglandin (PG) system in the regulation of renal NaCl excretion. In the present experiments, distal delivery of proximal tubular fluid (DD) [(C_H2O+C_cl)/GFR×100] and distal fractional chloride absorption (DFA_C1) [C_H2O/(C_H2O+C_α)] were studied in 6 healthy volunteers undergoing sustained water diuresis. Studies of renal function were performed during intravenous infusion of hypotonic (0.45%) saline and during additional treatment with indomethacin, furosemide and furosemide plus indomethacin. Hypotonic saline was infused at increasing rates of 0.09, 0.18, and 0.36ml min^-1 kg^-1 body weight each for a 45-min period. DD over all three clearance periods averaged 8.27 + 0.71 ml min^-1 100 ml^-1 glomerular filtration rate (GFR) during saline infusion alone and was unchanged by indomethacin (8.09 ± 0.63 ml min^-1100 ml^-1 GFR).DFA_C1averaged 0.79 + 0.02 during saline and significantly increased to 0.87 + 0.01 (p < 0.002) during concomitant indomethacin treatment. Increased NaCl absorption in the diluting segment during indomethacin was paralleled by a decrease in urinary excretion of chloride (U_C1V) from 221 + 29 during control to 124 ± 19 µEq/min (p < 0.025) and in urinary excretion of PGE₂ (U_PGE2V) from 1.45 + 0.12 to 0.51 + 0.09 pmol/min (p < 0.025). Furosemide increased U_PGE2V to 2.94 + 0.34 pmol/min (p < 0.05) and U_C1V to 2,590 + 128 µEq/min (p < 0.001). This effect was associated with an increase in DD to 26.70 + 1.33 ml min^-1 100 ml”¹ GFR (p < 0.001) and a decrease in DFA_Cl to 0.19 ± 0.02 (p < 0.001). Neither DD and DFA_Cl nor U_ClV were altered during furosemide+indomethacin as compared to furosemide in spite of a marked suppression of U_PGE2V to 0.56 ± 0.13 pmol/min. Our results support the concept that renal PG participate in the regulation of NaCl absorption in the diluting segments of the nephron. Furthermore, the tubular effects of furosemide appear not to be mediated by the PG system.

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Section: Urinary Pge2 Excretioncontrasting

confidence: 55%

Section: Introductionmentioning

confidence: 99%

Prostaglandins Participate in the Regulation of NaCl Absorption in the Diluting Segments of the Nephron in vivo: Effects of Furosemide

Düsing¹,

Nicolas²,

Glänzer³

et al. 1982

Kidney Blood Press Res

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“…Also in favor of our findings is the study of Kramerst al. [9], who studied urinary osmolality and free-water reabsorption under spironolactone alone and spironolactone plus a prostaglandine inhibitor (indomethacin).…”

Section: Discussionmentioning

confidence: 99%

Intrarenal Sodium Handling during Chronic Spironolactone Treatment

Roos¹,

Mees²,

Koomans³

et al. 1984

Nephron

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Intrarenal sodium handling was studied in 8 patients with essential hypertension before spironolactone treatment (200 mg/day), on the 4th day of treatment, and after 3 months of treatment. The results were compared with similar studies with chlorthalidone (50 mg/day). Renal sodium handling was assessed by simultaneous determination of the glomerular filtration rate, sodium, and potassium excretion, and maximal free-water clearance (CH₂O). We took CH₂O as an index of’distal’ sodium chloride reabsorption from which the proximal sodium reabsorption was calculated. During the first days of spironolactone treatment a natriuresis and increase in urinary flow rate was found. It resulted in a decrease of the extracellular fluid volume amounting to 0.9 liters and a 2.5-fold increase in the plasma renin activity. Potassium excretion showed a small but significant rise. After 3 months, virtually the same degree of volume depletion was found, which was comparable to that obtained after 3 months of chlorthalidone treatment. CH₂O, as a fraction of glomerular filtration rate, decreased by 24% both after 3 days and 3 months, whereas proximal sodium reabsorption increased from 87.8 to 90.4% of the filtered load. CH₂O, corrected for the ‘distal’ delivery of sodium, decreased from 85.3 to 80.7%. These changes were nearly the same as those found after 3 months of chlorthalidone treatment. It is concluded from these calculated values that spironolactone inhibits sodium chloride reabsorption in the diluting segment of the nephron and that the resulting increase in sodium delivery or urinary flow to the potassium excretory site partly counteracts the blocking effect of spironolactone on this part of the nephron, thus increasing potassium excretion during the acute administration of this drug.

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“…3 Flupirtine is a new non-narcotic analgesic which is thought to act centrally rather than peripherally,4 and because it may be given to patients requiring treatment with frusemide it is important to know if it influences frusemide-induced diuresis.…”

Section: Introductionmentioning

confidence: 99%