Regarding ureteric obstruction (n unilateral ureteric obstruction UUO), which is CORRECT?A. In UUO, blocking nitric oxide (NO) release contributes to renal vasoconstriction
In UUO, both PGE2 and NO contribute to the net renal vasodilation that occurs early following UUO. Studies have shown that the increase in PGE2 and the vasodilation of the obstructed kidney is blocked by indomethacin, a prostaglandin synthesis inhibitor. TXA2 is an influential postobstructive vasoconstrictor that contributes to the continued reduction in GFR and RBF. Administration of TXA2 synthesis inhibitors to the obstructed kidney limits the reduction in RBF and GFR.
In contrast to the early robust renal vasodilation with UUO, there is a modest increase in RBF with BUO that lasts approximately 90 minutes, followed by a prolonged and profound decrease in RBF that is greater than found with UUO. The shift seen with UUO of blood flow from outer to inner cortex is the opposite of that with BUO.
This difference between BUO and UUO could be due to an accumulation of vasoactive substances like ANP in BUO and this could contribute to preglomerular vasodilation and postglomerular vasoconstriction. Such substances do not accumulate in UUO because they would be excreted by the contralateral kidney.