The role of prostaglandins in the production of erythropoietin (ESF) by the kidney. II. Effects of indomethacin on erythropoietin production following hypoxia in dogs

Mujovic, Vujadin M.; Fisher, James W.

doi:10.1016/0024-3205(75)90267-2

Cited by 16 publications

(5 citation statements)

References 21 publications

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“…We have reported recently (4-6) that both hypoxic and ischemic hypoxia are capable of producing a significant increase in prostaglandin E (PGE) release into the renal venous effluent, which was blocked by the potent prostaglandin synthetase inhibitor, indomethacin. We have also demonstrated (7,8) that indomethacin is capable of blocking erythropoietin production as well.…”

mentioning

confidence: 81%

Enhanced Erythropoietin and Prostaglandin E Production in the Dog following Renal Artery Constriction

Gross

Mujovic²,

Jubiz

et al. 1976

Experimental Biology and Medicine

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The precise mechanism of erythropoietin (ESF) production and release from the kidney still remains obscure although it is well known that many forms of hypoxia, e.g., anemic, hypoxic, ischemic, and histotoxic, are capable of increasing erythropoietin production by the kidney (1). Recent observations (2, 3) indicate that following renal artery constriction in the dog, there is a release of prostaglandins (PG) into the renal venous blood. We have reported recently (4-6) that both hypoxic and ischemic hypoxia are capable of producing a significant increase in prostaglandin E (PGE) release into the renal venous effluent, which was blocked by the potent prostaglandin synthetase inhibitor, indomethacin. We have also demonstrated (7, 8) that indomethacin is capable of blocking erythropoietin production as well.Thus, the present studies were carried out to assess the relationship between PGE release and erythropoietin production by the kidney during a 12-hr ischemic hypoxic stimulus induced by means of renal artery constriction as well as the effects of indomethacin on these changes.Materials and methods. Twelve female mongrel dogs (six control and six indomethacin-treated) weighing 14.5-21 kg were used in this study. The animals were anesthetized with sodium pentobarbital (30 mg/ kg iv), and the left femoral arteries were cannulated for monitoring systemic arterial blood pressure (Statham P23AC pressure transducer) and the collection of arterial blood samples for erythropoietin bioassay. The animals were subjected to retroperitoneal laparotomies permitting extirpation of the right kidney and the exposure of the left kidney through a flank incision. A branch of the left ovarian vein was isolated and a cannula was inserted through this vein into the left renal vein to collect renal venous blood samples for PGE assay. Utilizing a squarewave electromagnetic blood flowmeter (Carolina Medical Electronics, Model 501) and either an 8-or 10-mm circumference flow probe, renal blood flow (RBF) was monitored with the probe placed around the left renal artery. Systemic arterial blood pressure (BP) and RBF were recorded continuously throughout the experimental period on a Grass oscillographic recorder (Model 7PCPA).After the initial zero time parameters (BP, RBF) and blood samples for PGE and erythropoietin were collected, a vascular occluder (Model OC12, IN VIVO Metric Systems) was placed around the left renal artery between the flow probe and the kidney. Renal blood flow was reduced to 30% of normal and sustained throughout the 12-hr experimental period with minor adjustments as needed. Six of the 12 dogs in the experimental group were pretreated with indomethacin (5 mg/kg orally) 18 and 2 hr prior to the application of the vascular occluder. Anesthesia was maintained throughout the experiments by administration of sodium pentobarbital as required via a cannula in the femoral vein.Blood samples for erythropoietin and 498

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mentioning

confidence: 81%

Enhanced Erythropoietin and Prostaglandin E Production in the Dog following Renal Artery Constriction

Gross

Mujovic²,

Jubiz

et al. 1976

Experimental Biology and Medicine

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“…Especially the prosta glandins of the E type have been demonstrated to exert direct effects on kidney production of EPO in the iso lated perfused kidney [2]. In addition EPO production by the kidney has been found to be blocked by the pros taglandin synthetase inhibitor drug indomethacin fol lowing ischemic and hypoxic hypoxia [2,5]. These find ings allow us to conclude that prostaglandins mediate a biological process which leads to the production of EPO.…”

Section: Discussionmentioning

confidence: 58%

Changes in Erythropoietin Serum Levels by Extracorporeal Shock Wave Lithotripsy

Vögeli

Schmitz‐Dräger²,

Mellin³

et al. 1990

Urol Int

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Erythropoietin (EPO) serum levels were measured in 30 patients before, during and immediately after shock wave treatment by an enzyme immunoassay. Shock wave treatment was performed in the Dornier lithotripter HM3 under a constant voltage of 18 kV. In 16 out of 30 patients, an increase in the EPO serum level of over 10 U/l more than the value obtained prior to the treatment was observed. Differences ranged from 11 to 50 U/l. In 3 patients EPO serum concentration after shock wave treatment rose above the physiological limit of 54 U/l. Increased EPO serum levels have been observed after applications both under and over 1,000 shock waves. The small number of cases does not allow a statistical correlation between the number of shock waves and the elevation of the EPO serum concentration. Further investigations are necessary to define the circumstances by which an increase in EPO serum level occurs under shock wave treatment.

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“…Unter denjenigen biochemischen Pa rametern, die eine Hypoxiereaktion vermitteln könnten, werden die Prostaglandine als ernsthafte Kandidaten betrachtet. Dies beruht auf folgenden Erkenntnissen: 1) verschiedene Gewebe, einschliesslich der Nieren, setzen auf Hypoxie hin mehr Prostaglandine frei [47,48]; 2) die Prostaglandine können die Bildung von EPO in der Nie re [49,50] und in Zellkulturen [51] stimulieren, und 3) die Hemmung der Prostaglandinbildung hemmt die durch CL-Mangel induzierte Bildung von EPO in vivo [21,52,53].…”

Section: Zelluläre Regulation Der Epo-produktionunclassified