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PubMedDate not supplied

[Effect of clonidine on polyuria induced by alcohol, water or the lack of vasopressin in the rat].

1. The effects of two doses of clonidine (100 and 500 micrograms/kg sc) were compared on several types of experimentally induced diuresis (total value during 4 hours): alcohol or water loaded rats and Brattleboro rats (i.e. animals with congenital lack of vasopressin). 2. The two doses of clonidine alone increased the values of urine flow (fig. 1 and 3). 3. Clonidine, at a low dosage (100 micrograms/kg sc), potentiated the increase in urine flow induced by water overloading but remained ineffective in alcohol--loaded rats (fig. 1). 4. Clonidine, at a higher dosage (500 micrograms/kg sc) reduced alcohol--or water--induced diuresis (fig. 3). 5. In Brattleboro rats, clonidine decreased urine flow (100 micrograms/kg sc) or was without effect (500 micrograms/kg sc) (fig. 2). 6. These results suggest that relatively high doses of clonidine may be useful in treatment of alcohol with drawal in man: the drug could act as a sympatholytic and sedative central agent but could also decrease alcohol--induced diuresis by inhibition of vasopressin release.

Animals↗
PubMed2001

Volume-induced natriuresis in healthy women: renal metabolism of prostacyclin and thromboxane, and physiological role of prostanoids.

In healthy women submitted to a short-term expansion in extracellular fluid volume we have evaluated the urinary excretory profile of the stable metabolites of prostaglandin(PG) I2 and thromboxane(TX) A2, 6-keto-PGF1 alpha(6KPGF) and TXB2 respectively, and assessed the physiological role played by the prostanoids in this experimental condition. Salt retention (SR group, n=9) was induced by repeated i.v. infusion of saline solution (0.9% NaCl). At the end of the treatment the body weight had increased by 0.7+/-0.2 kg (mean+/-SEM) (P<0.05). Renal functional exploration [clearance (cl.) method] was performed during hypotonic polyuria (induced by oral water load) and subsequent moderate antidiuresis (induced by low-dose infusion of an antidiuretic hormone analogue). Urinary 6KPGF and TXB2 concentrations were estimated by RIA method during polyuria (P cl. period), early and late antidiuresis (A1 and A2 cl. periods). Paired functional explorations were performed in absence (control study) and presence of indomethacin. Basal values of plasma sodium and potassium concentrations, plasma renin activity (PRA) and urinary aldosterone excretion were determined just before the control study. The results in salt retention were compared to those previously obtained in healthy women submitted to a moderate salt depletion (SD2 group, n=6), in absence and presence of the drug. Women in salt retention received 100 mg i.m. of the drug, whereas salt-depleted women received only a halved dose as in previous studies in salt depletion the full dose produced prolonged anuria. (I) Salt retention vs salt depletion. The basal values of PRA and urinary aldosterone excretion were significantly lower. During polyuria, urinary excretion of 6KPGF, 6KPGF/TXB2 ratio, urinary flow rate, creatinine cl. and absolute and fractional excretions of sodium and chloride were significantly higher. In salt retention during polyuria, significant positive correlations were found between 6KPGF excretion and functional excretory parameters. (II) Indomethacin in salt retention. The following effects were significant: (a) a reduction in prostanoid excretions in P and A1 cl. periods only; (b) during polyuria, an increase in arterial pressure, a reduction in urinary flow rate and creatinine cl. (saluresis showed not significant reduction). During polyuria significant positive correlations occurred between the absolute effects of indomethacin on 6KPGF excretion and those on functional excretory parameters. (III) Comparative effects of indomethacin in salt retention and salt depletion. Despite the double dosage of the drug, the significant reductions in urinary metabolite excretions were not significantly different during P cl. period and significantly lower in A1 cl. period compared to the corresponding significant reductions in salt depletion. During polyuria, the significant increase in arterial pressure was significantly different from the not significant effect in salt depletion; the not significant effect on saluresis was significantly different from the significant reduction in salt depletion. The results suggest the following conclusions: (1) The present model showed the functional pattern of the volume-natriuresis; (2) In salt retention, in contrast with salt depletion, indomethacin induced an increase in arterial pressure consistent with the inhibition of a PG-dependent vasodilator mechanism active at the systemic level; (3) In salt retention, in contrast with salt depletion, indomethacin failed to induce a significant reduction in saluresis. This failure can be attributed to the drug's blunted effectiveness in inhibiting the renal synthesis of saluretic PGs, and probably to the interference of the concurrent increase in arterial pressure in the renal treatment of sodium and chloride.

6-Ketoprostaglandin F1 alpha↗
PubMed1997

Urinary excretion of epidermal growth factor and Tamm-Horsfall protein in three rat models with increased renal excretion of urine.

Epidermal growth factor (EGF) and Tamm-Horsfall protein (THP) are synthesized in the kidneys by the distal tubular cells and excreted into urine. The urinary excretion of these peptides has been suggested as a potential index for distal tubular function. The urinary excretion rates of EGF and THP were examined in three groups of rats with increased renal excretion of urine: uninephrectomy, non-osmotic polyuria and diabetic osmotic polyuria. Twenty-four hour urine samples were obtained after 7, 14 and 21 days. The urinary volume per kidney was doubled in uninephrectomy when compared to controls. There was a seven-fold increase in urinary volume in rats with non-osmotic polyuria and diabetic osmotic polyuria, as compared to controls. Uninephrectomy, non-osmotic polyuria and diabetes all affected the urinary excretion of EGF and THP differently. The EGF excretion in uninephrectomized rats was 60-80% of that of the controls, whereas THP excretion was unchanged, indicating that EGF excretion varied with renal tissue mass. Non-osmotic polyuria caused a five-fold increase in THP excretion but no change in EGF excretion. THP excretion in the diabetic rats was increased three-fold after 21 days when compared to controls, whereas EGF excretion was decreased when expressed per kidney weight. Immunohistochemistry demonstrated that EGF and THP were colocalized in the thick ascending limbs of Henle's loops and distal tubules in all five groups of rats. In conclusion, the EGF excretion appears to follow renal tissue mass and seems independent of urinary volume, whereas THP excretion is dependent mainly on urinary volume. This has implications for the use of EGF and/or THP excretion rates as an indicator for distal tubular function.

Adjuvants, Immunologic↗
PubMed2003

Enuresis subtypes based on nocturnal hypercalciuria: a multicenter study.

PURPOSE: Desmopressin may not be effective for nocturnal enuresis associated with polyuria and hypercalciuria. Nighttime hypercalciuria in an enuretic population from 5 centers and its correlation with nighttime polyuria were verified. MATERIALS AND METHODS: A total of 450 enuretic patients (278 males, 172 females, mean age 9.7 years) were evaluated with 72-hour micturition charts, urinalysis, serum creatinine and osmolarity, diurnal and nocturnal electrolytes with fractional Na+ and K+ urinary excretion, and nocturnal (4 a.m.) plasma vasopressin. Creatinine electrolytes and osmolarity were measured in daytime (8 a.m. to 8 p.m.) and nighttime (8 p.m. to 8 a.m.) urine volumes. Patients were divided into group 1 with nocturnal polyuria and group 2 without nocturnal polyuria. Hypercalciuria was defined as urinary calcium-to-urinary creatinine ratio greater than 0.21. Statistic evaluation was performed using chi-square, Pearson correlation and ANOVA tests. RESULTS: Nighttime polyuria was demonstrated in 292 bedwetters (65% group 1). Nocturnal hypercalciuria was present in 179 of the 450 children (39.7%), including 125 in group 1 (42.8%) and 54 in group 2 (34.2%), which was statistically significant (chi-square p = 0.008, Pearson correlation test r = 0.157). Daytime calciuria was not statistically modified in either group (group 1 p = 0.054, group 2 p = 0.56). Adrenocorticotropic hormone (ADH) was normal in 18.5% and low in 81.5% of enuretics with nocturnal hypercalciuria. ADH levels and nocturnal hypercalciuria significantly correlated (p = 0.003, r = 0.148). Conversely, the group 2 patients had normal ADH levels. CONCLUSIONS: Nocturnal hypercalciuria has a pivotal role in nocturnal enuresis, as it is significantly associated with low ADH levels and nocturnal polyuria. A new classification of nocturnal enuresis subtypes based on nighttime calciuria levels is mandatory to address treatment properly.

Adolescent↗
PubMed1974

On the mechanism of lithium-induced diabetes insipidus in man and the rat.

The mechanism of lithium-induced diabetes insipidus was investigated in 96 patients and in a rat model. Polydipsia was reported by 40% and polyuria (more than 3 liter/day) by 12% of patients receiving lithium. Maximum concentrating ability after dehydration and vasopressin was markedly impaired in 10 polyuric patients and was reduced in 7 of 10 nonpolyuric patients studied before and during lithium therapy. Severe polyuria (more than 6 liter/day) was unresponsive to trials of vasopressin and chlorpropamide, but improved on chlorothiazide. Rats receiving lithium (3-4 meq/kg/day) developed massive polyuria that was resistant to vasopressin, in comparison to rats with comparable polyuria induced by drinking glucose. Analysis of renal tissue in rats with lithium polyuria showed progressive increase in the concentration of lithium from cortex to papilla with a 2.9-fold corticopapillary gradient for lithium. The normal corticopapillary gradient for sodium was not reduced by lithium treatment. The polyuria was not interrupted by brief intravenous doses of vasopressin (5-10 mU/kg) or dibutyryl cyclic AMP (10-15 mg/kg) capable of reversing water diuresis in normal and hypothalamic diabetes insipidus rats (Brattleboro strain). The present studies suggest that nephrogenic diabetes insipidus is a common finding after lithium treatment and results in part from interference with the mediation of vasopressin at a step distal to the formation of 3',5' cyclic AMP.

Animals↗