dinoprost and Dehydration

Brattleboro rats with hereditary diabetes insipidus make it possible to investigate effects of the urea concentration on the in vitro and in vivo production of prostaglandins E2 and F2 alpha (PGE2 and PGF2 alpha) by the renal papilla independently of any vasopressin effects. The rates of prostaglandin production in vitro are increasing between 100 and 1030 mmol/l urea and decreasing above 1030 mmol/l. The ratio PGE2/PGF2 alpha remains constant at about 4. Normally hydrated and 24 h water-deprived animals in steady state of urine formation were compared in vivo. Urine osmolality increased from 167 +/- 6 (N = 5) to 1113 +/- 35 (N = 15) mosmol/kg water and papillary urea concentration from 50 +/- 7 to 304 +/- 19 mmol/l after water deprivation. Urinary excretion rates of PGF2 alpha increased from 0.83 +/- 0.12 to 3.80 +/- 0.37 ng/h. The excretion of PGE2 was unaffected. PGE2 + PGF2 alpha excretion rates increased from 1.62 +/- 0.25 to 4.61 +/- 0.42 ng/h. These values are in accordance with values predicted from work with Sprague-Dawley rats. Together with previously published data on Sprague-Dawley rats these results indicate that variations of prostaglandin production in the conscious rat in steady state of urine formation can be accounted for by variations of plasma vasopressin and of papillary urea concentration. Variations in the excretion fraction are due to other causes.

Topics: Animals; Dehydration; Dinoprost; Dinoprostone; Kidney; Male; Osmolar Concentration; Rats; Rats, Brattleboro; Rats, Inbred Strains; Urea

The purpose of the study was to investigate the effects on urine flow and osmolar excretion of arachidonic acid (C20:4) infused in the renal artery of anaesthetized rats under conditions in which indomethacin previously was found to reduce urine flow and to prevent the development of a moderate saline diuresis. C20:4 caused a reversible increase in the urinary excretion rates of PGE2 and PGF2 alpha both in hydropenic rats and in rats during a saline diuresis. Renal venous plasma concentration of PGE2 increased significantly while the increase in PGF2 alpha was insignificant. C20:4 infusion was followed by an increase in urine flow and osmolar excretion rate in hydropenic rats, and it augmented urine flow (but not solute excretion) in saline-loaded rats. This latter effect was blunted by indomethacin treatment and inactin anaesthesia. Increased endogenous PG-levels were associated with only a modest (insignificant) increase in renin release under the present conditions. Saline loading acutely depressed PGE2 and PGF2 alpha urinary excretion rates and plasma renin concentration (PRC). The fall in PRC was unaffected by indomethacin. The main conclusions are that endogenous renal PG's have a diuretic effect in the amytal anaesthetized rat, while an effect on osmolar excretion rate is apparent only under hydropenic conditions. Acute saline loading depresses renal PG-synthesis, but this depression is not the only cause of the fall in PRC following saline loading. The saline diuresis is caused by a mechanism(s) not involving prostaglandins.

Topics: Anesthesia; Animals; Arachidonic Acid; Arachidonic Acids; Dehydration; Dinoprost; Dinoprostone; Male; Prostaglandins; Prostaglandins E; Prostaglandins F; Rats; Rats, Inbred Strains; Renin; Sodium Chloride; Stimulation, Chemical