The influence of dietary sodium on urinary prostaglandin excretion

Davila, D.; Davila, Tatjana; Oliw, Ernst H.; Änggård, Erik

doi:10.1111/j.1748-1716.1978.tb06195.x

Cited by 49 publications

(17 citation statements)

References 15 publications

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“…Factors such as urinary volume 21 and sodium excretion 40 have been reported to affect PGEj excretion, but, in contrast, in our experiments these variables did not correlate with U6kV. However, while it is generally recognized that urine PGF^ is mostly of renal origin, no comparable data exist for 6-ketoPGF, 0 .…”

Section: Response To Secretincontrasting

confidence: 55%

Furosemide increases urine 6-keto-prostaglandin F1 alpha. Relation to natriuresis, vasodilation, and renin release.

Wilson

Loadholt²,

Privitera³

et al. 1982

Hypertension

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SUMMARY While previous studies have shown that prostaglandins (PG) mediate the renal vasodilating and renin-releasing actions of furosemide, the dose-response relationship has not been defined nor has the specific PG involved. Prostacyclin (PGIj) is synthesized in the renal cortex, is a vasodilator, can release renin and, therefore, could mediate these actions of furosemide. The authors measured urinary excretion of the PGI 2 hydrolysis product 6-keto prostaglandin F la (U6kV) in response to increasing intravenous bolus doses of furosemide in anesthetized dogs.

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Section: Response To Secretincontrasting

confidence: 55%

Furosemide increases urine 6-keto-prostaglandin F1 alpha. Relation to natriuresis, vasodilation, and renin release.

Wilson

Loadholt²,

Privitera³

et al. 1982

Hypertension

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“…4). A variety of factors beside ADH are related to renal PGE 2 formation (NaC1 [11,51] and KC1 [16,53] balance, adreno-cortical hormones [63] and bradykinin [9]. These factors could, therefore, contribute to the renal response to ADH.…”

Section: Prostaglandins and The Control Of Electrolyte Balance And Urmentioning

confidence: 99%

Synthese und Wirkungen von Prostaglandinen in der Niere

et al. 1979

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The kidney has a high capacity to produce a spectrum of different acting prostaglandins (PG). In vivo and in vitro studies have shown that renal formation of PG's, possibly in the vasculature of the cortex represents an essential step in the mechanisms regulating the secretion of renin. PG's formed in the cortex seem to participate also in the control of renal vascular resistance and glomerular filtration rate. PGE2 formed in the medulla modulates the hydroosmotic action of antidiuretic hormone and influences the kidney's capacity for urine concentration. Renal PG formation is reduced by high NaCl intake and enhanced by low NaCl intake and in hypokalemic states. These findings make renal PG's good candidates for participation in the regulation of salt and water balance and in the control of blood pressure. Due to the close connection with the renin angiotensin system, alterations in renal PG formation might be involved in the etiology of high and low renin states. Thus, an impairment in the renal cortical production of vasodilating and renin-stimulating PG's could constitute the common denominator for both the reduced renin secretion and the increased vascular resistance which have been reported to be associated in essential hypertension.

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“…Most studies have dealt with animal models and the results have been conflicting (Zusman, Spector, Cadwell, Speroff, Schneider & Mulrow, 1973;Papanicolaou, Safer, Hornych, Fontaliran, Weiss, Bariety & Milliez, 1975;Tobian & O'Donnell, 1976;Weber, Larsson & Scherer, 1977;Davila, Davila, Oliw & Anggard, 1978;Lifschitz, Patak, Radem & Stein, 1978). We therefore decided to study the effects of changes in Na balance on the urinary excretion of prostaglandin E 2 and prostaglandin F 2a (PGE 2 and PGF 2a respectively) that reflect the renal synthesis of these prostaglandins (Frolich, Wilson, Sweetman, Smigel, Nils, Carr, Waston & Oates, 1975;Dunn & Hood, 1977).…”

Section: Introductionmentioning

confidence: 97%

Effect of Chronic and Acute Changes in Sodium Balance on the Urinary Excretion of Prostaglandins E2 and F2α in Normal Man

et al. 1981

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1. The effects of changes in sodium balance on renal prostaglandins have been hitherto studied mainly in experimental animals and the results have been controversial. In this study the 24 h urinary excretion of prostaglandins E2 and F2 alpha was measured by radioimmunoassay in seven normal subjects under basal conditions and after 5 days of a diet containing less than 20 mmol of sodium/day. Subsequently a sodium chloride (150 mmol/l: saline) load (300 mmol of sodium over 4 h) was infused and prostaglandins were again measured in hourly urine collections. Plasma renin activity and aldosterone were also measured under basal conditions, after the low sodium diet and at 2 and 4 h of the saline infusion. 2. Dietary sodium restriction was associated with a marked increase in prostaglandin E2 excretion (from 769.7 +/- 201.6 SEM to 1761.3 +/- 304.9 ng/24 h, P less than 0.0005). Prostaglandin F2 alpha also increased from 1187.0 +/- 390.1 to 1435.6 +/- 344.6 ng/24 h, but this was not statistically significant. The prostaglandin E2/prostaglandin F2 alpha ratio increased from 0.83 +/- 0.2 to 1.52 +/- 0.34 (P less than 0.01). Plasma renin activity and aldosterone rose significantly (P less than 0.05 and less than 0.0025 respectively). 3. During the saline load prostaglandin E2 decreased after 2 h from 142.4 +/- 29.9 to 86.7 +/- 22.9 ng/h (P less than 0.05) and to 36.9 +/- 5.96 ng/h after 4 h. Prostaglandin F2 alpha decreased at a slower rate, from 98.4 +/- 18.7 to 37.5 +/- 8.8 ng/h at 4 h (P less than 0.02). At 4 h the prostaglandin E2/prostaglandin F2 alpha ratio returned to control values (0.90 +/- 0.17). Plasma renin activity and aldosterone decreased significantly after 2 h (P less than 0.02 and less than 0.0025 respectively) and reached control values after 4 h. 4. The present study demonstrates that chronic and acute changes in sodium balance induce changes in the excretion of prostaglandin E2 parallel to changes in plasma renin activity and aldosterone. The similar but quantitatively smaller changes in prostaglandin F2 alpha and the inversion of the ratio between the two prostaglandins during sodium deprivation suggest that at least two factors are involved: increased delivery of substrate for prostaglandin synthase and decreased activity of the prostaglandin E1 9-keto-reductase. Prostaglandins probably play an important role in the adaptation of the kidney to changes in sodium balance.

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The influence of dietary sodium on urinary prostaglandin excretion

Cited by 49 publications

References 15 publications

Furosemide increases urine 6-keto-prostaglandin F1 alpha. Relation to natriuresis, vasodilation, and renin release.

Furosemide increases urine 6-keto-prostaglandin F1 alpha. Relation to natriuresis, vasodilation, and renin release.

Synthese und Wirkungen von Prostaglandinen in der Niere

Effect of Chronic and Acute Changes in Sodium Balance on the Urinary Excretion of Prostaglandins E2 and F2α in Normal Man

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