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Role of sodium depletion in acute antidiuretic effect of bendroflumethiazide in rats with nephrogenic diabetes insipidus.

The mechanisms underlying the acute antidiuretic response to bendroflumethiazide (BFTZ; 0.25 mg/h for 3 h) in rats with nephrogenic diabetes insipidus (NDI) was investigated. NDI was induced in conscious chronically instrumented female Wistar rats either by chronic lithium administration (40-60 mmol Li/kg of diet for 4 weeks) or by acute infusion of V2 antagonist OPC-31260 (0.2 mg/h). Renal clearance experiments were performed in conscious rats instrumented with permanent catheters. During experiments total body water content was held constant by i.v. replacement of urine production (V) with 150 mM glucose. One group in addition received i.v. replacement of urinary sodium losses. In both models of NDI, BFTZ-induced antidiuresis was associated with a decrease in the delivery of tubular fluid to the distal nephron, as measured by lithium clearance (C(Li)). Both the antidiuresis and the decrease in C(Li) could be prevented by sodium replacement. BFTZ did not affect distal water handling as measured by V/C(Li). BFTZ did not induce antidiuresis in normal rats with water diuresis. It is concluded that in rats with NDI, thiazide-induced antidiuresis can be entirely explained by a fall in distal delivery of tubular fluid related to sodium depletion. This contrasts the response in rats with central diabetes insipidus, where thiazides in addition increase distal water reabsorption.

Animals↗

[Effect of furosemide on the intrarenal hemodynamics and excretory renal function depending on salt regime].

The experiments on rats showed that the dietary mineral composition influences renal circulation and saluretic function and modifies the related effects of furosemide. In particular, a high NaCl intake reduces the blood perfusion in the renal cortex and increased that in the renal medulla, thus increasing sodium excretion with urine. The use of hyposol, a table salt substituent, enhances the blood flow in the renal medulla and leads to a significant increase in the diuresis, natriuresis, and kaliuresis. Furosemide (10 mg/kg) sharply increases the medullar circulation and electrolyte excretion on the background of standard diet. However, these effects were much less pronounced on the background of hypersodium diet or hyposol administration.

Animals↗

[Development of renal function in low and extremely low birth weight infants: correlation with gestational and postnatal age].

The postnatal development of renal function was compared in 29 infants with a gestation age (GA) of 26-30 weeks mean 28.5 680-1,450 g means 1080 g and in 31 infants with a gestation age of 31-33-weeks, means 31.5, 950-2000 g means 1580 g. Observation were made during the 1st, 5th and 10th day. From 1st to 10th day the creatinine clearance increased but it was significantly lower in GA 26-30 that in GA 31-33. During the first 10 days of life diuresis was lower in GA 26-30 that in GA 31-33 but thereafter was the same in both groups. Urinary sodium excretion was high at 1st and 5th day in both groups and decreased with increasing postnatal age. Na excretion was slightly higher in GA 26-30 that in GA 31-33 at 1st and 5th day but not at 10th day. UK/UNa was below 1 in both groups during the 1st, 5th day and increased with postnatal age. FeNa% was high in both groups but in GA 26-30 was significantly hither then in GA 31-33. We conclude that the postnatal development of renal function is retarded in all preterm infants and is slightly slower in infants with a GA below 31 weeks than in infants with GA 31-33 weeks.

Creatinine↗