A partial obstruction of the left ureter was created in weanling (3-week-old) rats. Renal function was studied after 7-9 weeks and compared to that in age-matched controls. Arterial blood pressure was found substantially increased. During normal hydration, the hydronephrotic kidney had low excretions of urine, potassium, osmoles and, especially, sodium. The contralateral, intact side showed no compensatory traits. On volume expansion, the hydronephrotic kidney demonstrated an unimpaired reacting capacity, leading to normalization of urine, sodium and osmole excretions and even to supernormal renal blood flow, glomerular filtration and potassium excretion. On the intact side, the excretion of potassium was increased like that on the hydronephrotic one, while excretions of urine, sodium and osmoles were increased even more. The fact that the intact kidney handled most of the urine excretion was interpreted as the result of a mechanism protecting the obstructed kidney from additional pressure insults while homeostasis was maintained. The arterial hypertension may result from the combination of retention of fluid and sodium by the hydronephrotic kidney and the absence of compensation by the intact kidney during normal hydration – like that in everyday life. The functional changes during normal hydration were generally more severe than those we found after obstruction in neonatal and adult rats, in which arterial hypertension was never observed. The clinical implication would be that the kidney may be less tolerant to pressure rises during the infant year. Changes due to obstruction are known to occur rapidly, but after that neither progress nor reverse. It therefore seems advisable to intensify the monitoring during this sensitive period of antenatally detected cases, selected for nonoperative follow-up according to modern principles, in order to detect sudden amplifications of their congenital obstruction.

Keywords:
Hydronephrosis, experimental, Weanling rats, Partial ureteric obstruction, Renal function, Arterial blood flow
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© 1992 S. Karger AG, Basel
1992
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