Efecto de un incremento en la diuresis sobre la absorción y retención de algunos nutrientes en ratas / Effect of an increase in diuresis on absorption and retention of some nutrients in rats

Estudios previos en ratas han demostrado que la administración del diurético furosemida aumenta la pérdida urinaria de electrolitos y nutrientes, causando un efecto negativo sobre las reservas de los mismos. Una alternativa para proteger esas reservas es incrementar la absorción intestinal. Así, se evaluó la absorción, pérdidas urinarias y reservas corporales de nitrógeno, calcio, magnesio, sodio, potasio y cinc, en cuatro grupos de ratas: control, y tres grupos experimentales que consumieron furosemida en concentraciones de 0,5; 1,0 y 1,5 mg/g de dieta, durante 23 días. El diurético causó poliuria dosis dependiente, disminución en el consumo de alimento, la eficiencia y el crecimiento. También, provocó un aumento en las pérdidas urinarias del nitrógeno y minerales. La absorción de nitrógeno, calcio y cinc no se modificó, mientras que la del magnesio, sodio y potasio aumentó ligeramente. Se determinó que la absorción no compensó las pérdidas urinarias. Así, la furosemida afectó negativamente la retención de nutrientes y electrolitos, provocando una reducción en las reservas corporales de los mismos. Este diurético tiene un efecto negativo sobre el estado nutricional en ratas, causado por la reducción en el consumo de alimento, así como en la utilización de los nutrientes consumidos. La reducción en la utilización de los nutrientes asociada con este diurético, puede ser explicada en parte, por una pobre retención de nutrientes por el riñón, que no puede ser compensada por un incremento en la absorción intestinal.

Previous studies have shown that, in rats, the administration of the diuretic furosemide increases diuresis as well as urinary loss of electrolytes and essential nutrients. This loss has a negative effect on electrolytes and nutrient reserves. Since one alternative to help protect these reserves is to increase intestinal absorption, the purpose of this study was to evaluate the absorption, urinary loss and tissue reserves of nitrogen, calcium, magnesium, sodium, potassium and zinc in rats offered 0, 0.5, 1.0 and 1.5 mg furosemide per g diet, daily during 23 days. The diuretic caused a dose dependent polyuria, a reduction in food intake, growth and feed efficiency. In addition, those rats had increased urinary loss of nitrogen and minerals. Nitrogen, calcium and zinc absorption were not affected, but magnesium, sodium and potassium increased slightly. Intestinal absorption could not compensate for urinary loss. In general, this study showed that in rats, this diuretic had a negative effect on nutritional status caused by a reduction in food intake and also in the utilization of the nutrients consumed. The reduction in nutrient utilization associated with this diuretic may be partly explained by a poor nutrient retention by the kidney which was not compensated by an increase in intestinal absorption.

Effect of bafilomycin on proximal bicarbonate absorption in the rat

To evaluate the relative importance of the V-type H(+)-ATPase in proximal bicarbonate reabsorption in vivo, proximal tubules of male and female Wistar rats (180 to 260 g) were perfused with bicarbonate-Ringer solution with and without the addition of 2 microM bafilomycin A1. Bafilomycin significantly increased stationary pH from 6.75 +/- 0.05 (N = 39) to 6.86 +/- 0.03 (N = 82), the stationary concentration of bicarbonate from 5.24 +/- 0.62 to 6.33 +/- 0.46 mM and the half-time of acidification from 3.72 +/- 0.22 to 4.65 +/- 0.25 s, and significantly decreased net bicarbonate reabsorption from 3.17 +/- 0.21 to 2.55 +/- 0.15 nmol s-1 cm-2, that is, by 20 per cent . Since bafilomycin is considered to be a specific inhibitor for V-type H(+)-ATPase, these data establish 1) the existence of this type of transport in the rat proximal tubule and 2) that approximately a fifth of the total proximal bicarbonate reabsorption is due to this mechanism of transport

Effect of glucose on the kinetics of bicarbonate reabsorption in the early and middle proximal tubule

The kinetics of bicarbonate reabsorption in the early (EPT) and middle proximal tubule (MPT) was studied in Munich Wistar rats by means of microperfusion techniques. The early proximal tubule (EPT) had a higher capacity of reabsorbing bicarbonate than the middle segment. The calculated bicarbonate flow (JHCO3) was 4.47 nmol s**-1 cm**-2 int the EPT and 2.30 nmol s**-1 cm**-2 in the MPT and the half time of injected bicarbonate (t/2) was less in the EPT (2.24 s) than in the MPT (5.20 s). The presence of 20 mM glucose in the lumen led to a reduction in the velocity of tubular acidification in the EPT (3.11 s) and caused a decrease in JHCO3 in both segments (2.46 nmol s**-1 cm**-2 in the EPT and 1.64 nmols s**-1 cm**-2 in the MPT). These alterations may be the result either of lumen-to-cell sodium gradient dissipation or electrical changes induced by sodium-glucose cotransport that may depolarize the basolateral membrane leading to intracellular alkalinization. This effect may then impair the Na +/H+ exchanger, thus decreasing bicarbonate reabsorption