Figure 836

Acute renal hemodynamic response to unilateral or bilateral complete ureteral obstruction. In the first 2 hours after unilateral complete ureteral obstruction, there is a reduction in preglomerular vascular resistance and an increase in renal blood flow mediated by increased production of prostaglandin E2 (PGE2), prostacyclin, and nitric oxide (NO). The increase in renal blood flow (RBF) and glomerular capillary pressure maintain the glomerular filtration rate (GFR) at approximately 80% of normal, despite an increase in intratubular pressure. As the ureteral obstruction persists, activation of the renin-angiotensin system and increased production of thromboxane A2 (TBXA2) and endothelin result in progressive vasoconstriction, with reductions in renal blood flow and glomerular capillary pressure. The glomerular filtration rate decreases to approximately 20% of baseline, despite normalization of the intratubular pressures. The hemodynamic changes in the early phase (0-2 h) of bilateral ureteral obstruction are similar to those observed after unilateral obstruction. As bilateral obstruction persists, however, there is an accumulation of atrial natriuretic peptide (ANP) that does not occur after unilateral obstruction. The increased ANP levels attenuate the afferent and enhance the efferent vasoconstrictions, with maintenance of normal glomerular capillary and elevated tubular pressures. Despite these differences in hemodynamic changes between unilateral and bilateral ureteral obstruction, the reductions in renal blood flow and glomerular filtration rate 24 hours after obstruction are similar [47-49]. Pgc—glomerular capillary hydraulic pressure; PGI2—prostaglandin I2; Pt—tubule hydrostatic pressure; Ra—afferent arteriolar resistance; Re—efferent arteriolar resistance.

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