It is suggested that in patients with CRF who experience a decrease in the glomerular filtration rate (to 75-90% of the normal value) the increase in urine flow is due to prostaglandin-dependent inhibition of ion reabsorption in the thick ascending limb of the loop of Henle.

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We found an experimental solution to the paradox when the reabsorption of solute-free water increases with a simultaneous increase in diuresis and saluresis in the rat kidney under the oxytocin action. Injection of oxytocin to rats (0.25 nmol/100 g of body weight) increases diuresis from 0.16 ± 0.03 to 0.26 ± 0.02 mL/h, the excretion of solutes from 134 ± 13.7 to 300 ± 16.3 μOsm/h, and the reabsorption of solute-free water, which correlates with the renal excretion of oxytocin (p < 0.001). The mechanism of the effect is that oxytocin decreases the reabsorption of ultrafiltrate in the proximal tubule (the clearance of lithium increases) and increases the fluid flow through the distal segment of the nephron. In vivarium rats, urine osmolality (1010 ± 137 mOsm/kg H2O) and the concentration of vasopressin are high, this causes an increase in the reabsorption of solute-free water. Thus, oxytocin increases saluresis, which, against the background of a high level of endogenous vasopressin, increases the water reabsorption in the collecting ducts.

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