Pathophysiology of hydronephrotic atrophy: the cause and role of active preglomerular vasoconstriction

Unilateral complete ureteral occlusion is followed by a decreased blood flow in the ipsilateral kidney, which is established within 1 week, after which a steady state of whole renal blood flow is observed. Active preglomerular vasoconstriction is assumed to be the main factor causing renal flow reduction in the hydronephrotic kidney, resulting in rapid decrease of the initial elevated pelvic pressure within 24 h. The assumption of active preglomerular vasoconstriction also explains the observation that blood flow reduction clearly precedes renal atrophy after ureteral ligation. Neither alpha-receptor blocking agents nor angiotensin II blockage, nor denervation, reversed flow reduction in the first hours or weeks after ureteral ligation. A thromboxane synthesis inhibitor (imidazole) did reverse flow reduction completely without affecting the contralateral renal blood flow, indicating that active vasoconstrictive is present. In respect to renal hydronephrotic atrophy, compartment analysis of the blood flow of the obstructed kidney demonstrates that vasoconstriction contributes to ischemic atrophy at least in the cortex of the hydronephrotic kidney. Vasoconstriction cannot be reversed by prostaglandin synthesis inhibition after renal atrophy is established, although the renal blood flow is still sensitive to other vasodilating drugs like dopamine. From our data we conclude that prostaglandin-mediated active preglomerular vasoconstriction is a main factor causing renal atrophy by ischemia.