PGI2 synthesis and excretion in dog kidney: evidence for renal PG compartmentalization

Boyd, R. M.; Nasjletti, A.; Heerdt, Paul M.; Baer, Philip G.

doi:10.1152/ajprenal.1986.250.1.f58

Cited by 8 publications

(7 citation statements)

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“…There is no evidence for tubular secretion of 6-keto-PGF1,. Stop flow experiments (Boyd et al 1986) indicate that 6-keto-PGF1, is not added to the urine beyond the glomerulus. Urinary excretion of 6-keto-PGF,, is not influenced by inhibition of the organic acid secretory pathway with probenecid (Rosenkranz et al.…”

Section: Discussionmentioning

confidence: 99%

Renal degradation and distribution between urinary and venous output of prostaglandins E₂ and I₂

Bugge

Vikse

Dahl

et al. 1987

Acta Physiologica Scandinavica

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To examine renal degradation and distribution between urine and renal venous blood, prostaglandins E2 and I2 (PGE2 and PGI2), and a metabolite of PGI2, 6-keto-PGF1 alpha, were infused into the suprarenal aorta of anaesthetized dogs after blocking prostaglandin synthesis by indomethacin, 10 mg kg-1 body wt iv. During one passage through the kidney 80% of PGE2 and only 25% of PGI2 and 6-keto-PGF1 alpha were metabolized. Prostaglandin degradation and arterial input were proportional (r greater than 0.90). To stimulate the intrarenal prostaglandin synthesis in unblocked kidneys, arachidonic acid was infused at rates ranging from 24 to 160 micrograms min-1 kg-1 body wt. During arachidonic acid and PGE2 infusion the urinary excretion of PGE2 was about 20% of the renal venous output over a wide range of infusion rates. During arachidonic acid and PGI2 infusion urinary excretion of 6-keto-PGF1 alpha was about 10% of total renal output, but failed to increase further when total renal output exceeded 70 pmol min-1. Further increase in output occurred only in the renal vein. In contrast, during 6-keto-PGF1 alpha infusion the urinary excretion and the renal venous output of this metabolite were related as 1:2 over a wide range of infusion rates. Thus, PGI2 is much less degraded by renal tissue than PGE2, and the distribution patterns differ. Similar distributions between urine and renal venous blood during aortic infusion and stimulated intrarenal synthesis suggest a pre-glomerular vascular origin of both prostaglandins.

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Section: Discussionmentioning

confidence: 99%

Renal degradation and distribution between urinary and venous output of prostaglandins E₂ and I₂

Bugge

Vikse

Dahl

et al. 1987

Acta Physiologica Scandinavica

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“…The notion that cyclooxygenase plays a role in the renal vasodilatory effect of heme is reinforced by the finding that heme increases the urinary excretion of 6-keto-PGF 1␣ , the inactive derivative of PGI 2 . As PGI 2 is known to promote renal vasodilation, 17 the renal vasodilatory effect of heme is attributable to an enhanced production of renal PGI 2 . This conclusion fits well with the results of a previous study documenting that heme promotes prostaglandin production in cultured endothelial cells.…”

Section: Effects Of Intravenous Administration Of Heme In Rats Pretrementioning

confidence: 99%

Effects of Exogenous Heme on Renal Function

et al. 2003

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Abstract-We examined the effects of heme administration (15 mg/kg IV) on indexes of renal carbon monoxide production and contrasted the renal functional response to heme in anesthetized rats pretreated and not pretreated with stannous mesoporphyrin (40 mol/kg IV) to inhibit heme oxygenase or sodium meclofenamate (5 mg/kg IV plus infusion at 10 g/kg per minute) to inhibit cyclooxygenase. In rats without drug pretreatment, heme administration decreased renal vascular resistance and increased renal blood flow, urine volume, and sodium excretion associated with augmented urinary excretion of 6-keto-PGF 1␣ and enhanced concentration of carbon monoxide in the renal cortical microdialysate. Pretreatment with stannous mesoporphyrin did not prevent heme from producing renal vasodilation and increasing renal blood flow but abolished the diuretic and natriuretic responses. Conversely, pretreatment with sodium meclofenamate blunted the renal vasodilatory effect of heme but affected neither the diuretic nor the natriuretic effect. We conclude that heme-induced renal vasodilation is a cyclooxygenase-dependent response involving increased synthesis of PGI 2 , whereas heme-induced diuresis and natriuresis are heme oxygenase-dependent responses involving inhibition of tubular reabsorption of sodium and water through undefined mechanisms.

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“…1986). Boyd et al (1986) recently examined the compartmentalization of renal PG synthesis and excretion in vivo in canine kidneys. Their results with AA and bradykinin as agonists are in agreement with the present findings; they concluded that "in the dog PGE2 synthesized in the kidney enters directly into both the renal vascular and tubular compartments, but 6-keto-PGFI , of renal origin enters directly into only the renal vascular compartment."…”

Section: Discussionmentioning

confidence: 99%

Renal Prostaglandin Efflux Induced by Vasopressin, Ddavp and Arachidonic Acid: Contrasting Profile and Sites of Release

Miller

Westlin

McNeill

et al. 1986

Clin Exp Pharma Physio

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Prostaglandin (PG) efflux into ureteral (UE) and venous effluents (VE) of rabbit isolated perfused kidneys was determined by superfusion bioassay and radioimmunoassay (RIA), in response to injections of arginine-vasopressin (AVP), the non-pressor vasopressin analogue 1-deamino-8-D-arginine vasopressin (dDAVP) and arachidonic acid (AA). dDAVP (10-1000 ng) failed to stimulate renal PG release, whereas AVP (10-100 ng) and AA (10-50 micrograms) caused a dose-dependent release of PG. AVP evoked PG release into both effluents with release into the VE greater than UE at high doses. In contrast, PG release by AA was almost exclusively into the VE. Indomethacin (2.8 X 10(-6) mol/l) abolished AVP- and AA-induced PG efflux in both effluents, and vasodepressor responses to AA. PGE2 was the predominant PG released in response to AVP in both effluents whereas AA released primarily 6-keto-PGF1 alpha. The contrasting sites and profile of released PG suggest that exogenous AA and AVP stimulate the release of PG from different regions/cell types within the kidney.

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PGI2 synthesis and excretion in dog kidney: evidence for renal PG compartmentalization

Cited by 8 publications

References 0 publications

Renal degradation and distribution between urinary and venous output of prostaglandins E₂ and I₂

Renal degradation and distribution between urinary and venous output of prostaglandins E₂ and I₂

Effects of Exogenous Heme on Renal Function

Renal Prostaglandin Efflux Induced by Vasopressin, Ddavp and Arachidonic Acid: Contrasting Profile and Sites of Release

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PGI2 synthesis and excretion in dog kidney: evidence for renal PG compartmentalization

Cited by 8 publications

References 0 publications

Renal degradation and distribution between urinary and venous output of prostaglandins E2 and I2

Renal degradation and distribution between urinary and venous output of prostaglandins E2 and I2

Effects of Exogenous Heme on Renal Function

Renal Prostaglandin Efflux Induced by Vasopressin, Ddavp and Arachidonic Acid: Contrasting Profile and Sites of Release

Contact Info

Product

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Renal degradation and distribution between urinary and venous output of prostaglandins E₂ and I₂

Renal degradation and distribution between urinary and venous output of prostaglandins E₂ and I₂