High urine flow rate increases prostaglandin E excretion in the conscious dog

Wright, Lucius F.; Rosenblatt, Steven G.; Lifschitz, Meyer D.

doi:10.1016/0090-6980(81)90051-4

Cited by 22 publications

(20 citation statements)

References 8 publications

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“…Studies in which both renal venous and urinary prostaglandin E were measured demonstrated parallel changes in both, but quantitatively more prostaglandin E was found excreted in the urine (Dunn et al, 1978). Although it has been suggested that urinary flow rate is a major determinant of urinary prostaglandin E excretion (Wright & Lifschitz, 1979), previous studies from our laboratory have shown that the increase in urinary prostaglandin E during immersion is not solely a function of increased urine flow rate, but rather reflects increased renal prostaglandin E production (Epstein et al, 1979).…”

Section: Discussionmentioning

confidence: 96%

Dissociation of Renin-Aldosterone and Renal Prostaglandin E during Volume Expansion Induced by Immersion in Normal Man

et al. 1980

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The relationship of the renin--angiotensin--aldosterone axis with renal prostaglandin E is complex. Although studies have suggested that these two hormonal systems respond to experimental manipulations in a parallel manner, their interdependence has not been assessed fully during volume expansion. Since studies have demonstrated that in normal man the central hypervolaemia induced by water immersion to the neck produces a prompt and profound suppression of plasma renin activity and plasma aldosterone concentration without concomitant alteration of plasma composition, immersion afforded a unique opportunity to assess simultaneously the effects of central hypervolaemia on plasma renin activity, plasma aldosterone concentration and prostaglandin E excretion. 2. Seven normal subjects were studied twice while in balance on a diet containing 10 mmol of sodium/day, 100 mmol of potassium/day: with indomethacin administration (50 mg given every 6 h for five doses) and without indomethacin. Urinary prostaglandin E excretion was measured hourly and plasma renin activity and plasma aldosterone concentration at 30 min intervals. 3. Immersion was associated with a marked suppression of plasma renin activity (59 +/- 7%) and plasma aldosterone concentration (55 +/- 3%) with a return to pre-study values during the recovery hour. Concomitantly, urinary prostaglandin E excretion increased from 4.7 to a peak of 10.9 ng/min. Although administration of indomethacin lowered the basal rate of urinary prostaglandin E excretion and plasma renin activity, it did not prevent the subsequent augmentation of urinary prostaglandin E or the suppression of plasma renin activity and plasma aldosterone during the subsequent 4 h of immersion. 4. These results demonstrate a dissociation of renin--aldosterone and prostaglandin E during hypervolaemia and suggest that whereas prostaglandin E may constitute one of the major determinants of renin release clinically and experimentally, these two hormonal systems can be dissociated from each other in response to central volume expansion in man.

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Section: Discussionmentioning

confidence: 96%

Dissociation of Renin-Aldosterone and Renal Prostaglandin E during Volume Expansion Induced by Immersion in Normal Man

et al. 1980

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“…Pharmacologic studies by Olsen (24) indicate that clonidine increases urinary excretion of PGE, and indirect observations in our laboratory (14) suggest that exposure of the renal papilla may enhance renal PGE production. Unfortunately, both of these maneuvers are associated with an increase in urine flow rate, which has a direct relationship to PGE excretion (25,26). It is not clear, however, whether the increased PGE excretion reflects an increase in synthesis of the hormone.…”

Section: Discussionmentioning

confidence: 97%

“…That fractional sodium delivery to the early and late portion of superficial distal tubule (series III experiments) did not differ under these conditions excludes an effect of medullary tonicity on the LH and distal tubule of this nephron population. Fractional reabsorption by the papillary collecting duct was between 25 and 50% of the filtered load delivered to that segment. In view of similar findings in other natriuretic conditions (8-10, 17, 23), it seems unlikely that medullary tonicity influenced reabsorption by this segment.…”

Section: Discussionmentioning

confidence: 99%

Effect of Medullary Tonicity on Urinary Sodium Excretion in the Rat

Reineck¹,

Parma²

1982

J. Clin. Invest.

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A B S T R A C T In previous reports from this laboratory we have suggested that a reduction in medullary tonicity decreases the thin ascending loop of Henle sodium reabsorption and is in part responsible for the magnitude for the natriuresis accompanying 10% body weight Ringer loading. According to this postulate, one would expect that the medullary washout associated with water diuresis would also result in a natriuresis, but this does not occur. It is possible, however, that increased delivery from the proximal tubule is necessary to demonstrate an effect of medullary tonicity on urinary sodium excretion. Micropuncture studies were designed to test that possibility by increasing distal delivery by 2% Ringer loading in animals with and without reduced medullary tonicity. In an initial series of experiments the a-adrenergic agonist clonidine was used to induce a water diuresis. When given alone, this agent caused a marked decrease in urine osmolality and an increase in urine flow rate but had no effect on proximal reabsorption in either superficial or juxtamedullary nephrons, and did not alter urinary sodium excretion. Volume expansion with 2% body weight Ringer solution resulted in a significant fall in proximal reabsorption and a trivial increment in sodium excretion. When this same degree of volume expansion was conferred on animals undergoing a water diuresis, a marked increase in absolute and fractional sodium excretion occurred. In a second group of studies medullary tonicity was reduced in the left kidney only by removal of the left ureter 1 h before micropuncture. When these animals were infused with 2% body weight Ringer solution, proximal reabsorption was decreased in juxtamedullary nephrons, and a marked increase in sodium excretion was observed only from the left kidney. Finally, the effect of water diuresis on fractional sodium delivery to the early and late distal tubule of superficial nephrons during 2% Ringer loading was evaluated. Delivery to both of these sites was comparable after 2% Ringer loading alone and during 2% Ringer loading plus water diuresis.From these data, we conclude that medullary tonicity does influence renal sodium handling but that this effect is manifest in the final urine only under conditions in which proximal reabsorption is decreased. The data also suggest that this effect is limited to juxtamedullary nephrons and is probably localized to the thin ascending limb of the loop of Henle.

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“…In addition, aceta¬ zolamide, a carbonic anhydrase inhibitor which pro¬ duces metabolic acidosis but also makes the urine alka¬ line still increases the rate of PGE excreted in the urine . The flow-dependent nature of PGE excretion was first demonstrated in the conscious dog (Kirschen¬ baum & Serros, 1980) and in man (Kaye, Zipser, Hahn et al 1980), but this effect could not be reproduced in the anaesthetized dog (Wright, Rosenblatt & Lifschitz, 1981 ). In addition, it has been suggested that the rat is a species in which PGE excretion is independent of urine flow (Fejes-Toth, Fejes-Toth, Rigter & Frolich, 1983).…”

Section: Calculated Percentage Pge Reabsorbed Distallymentioning

confidence: 95%

Urine pH and the relationship between urine flow and urinary prostaglandin E excretion in the rat

Haylor¹,

Lote²

1986

Journal of Endocrinology

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The relationship between urine flow and urinary prostaglandin E (PGE) excretion was investigated at constant urine pH in the anaesthetized rat. The urine pH was maintained at approximately pH 6 or pH 8 by the intravenous infusion of either ammonium chloride or sodium bicarbonate respectively. Two distinct patterns in the relationship between PGE excretion and urine flow were observed. The first showed a fall in urinary PGE excretion as the urine flow increased over the low flow range of 2-5 ml/h, and was common to both experiments. The second relationship, however, showed a marked difference between the ammonium chloride and sodium bicarbonate experiments since: (a) in acidic urine (pH 6), PGE excretion increased (P less than 0.002) with the urine flow, attaining a rate of 87 +/- 6 pmol/h (n = 6) at the highest level of flow achieved (12 ml/h); (b) in alkaline urine (pH 8), PGE excretion was significantly (P less than 0.01) higher but did not increase with urine flow, remaining constant at approximately 90 pmol/h (n = 6). The lack of any additive effect on urinary PGE excretion between increasing the urine flow and making the urine alkaline may be explained by both stimuli acting through a common mechanism, a concept which is consistent with the hypothesis that PGE may be reabsorbed in the distal nephron. The flow-dependency of urinary PGE excretion could therefore result from a reduction in reabsorption rather than the increase in passive secretion proposed previously.(ABSTRACT TRUNCATED AT 250 WORDS)

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High urine flow rate increases prostaglandin E excretion in the conscious dog

Cited by 22 publications

References 8 publications

Dissociation of Renin-Aldosterone and Renal Prostaglandin E during Volume Expansion Induced by Immersion in Normal Man

Dissociation of Renin-Aldosterone and Renal Prostaglandin E during Volume Expansion Induced by Immersion in Normal Man

Effect of Medullary Tonicity on Urinary Sodium Excretion in the Rat

Urine pH and the relationship between urine flow and urinary prostaglandin E excretion in the rat

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