The Pathophysiology of Obstructive Nephropathy: The Role of Vasoactive Compounds in the Hemodynamic and Structural Abnormalities of the Obstructed Kidney

Vasoactive compounds such as angiotensin II, thromboxane A2, nitric oxide, and eicosanoids have a role in the hemodynamic and structural abnormalities that occur following obstruction of the urinary tract. Inhibition of angiotensin II and thromboxane synthesis increases glomerular filtration rate and renal plasma flow significantly in the postobstructed kidney. Angiotensin II also appears to mediate tubular interstitial fibrosis in the obstructed kidney. Indeed, use of angiotensin-converting enzyme inhibitors decreases the degree of interstitial fibrosis and the increased deposition of collagen seen in rats with prolonged ureteral obstruction. Vasoactive compounds such as angiotensin II, thromboxane A2, nitric oxide, and eicosanoids have a role in the hemodynamic and structural abnormalities that occur following obstruction of the urinary tract. Inhibition of angiotensin II and thromboxane synthesis increases glomerular filtration rate and renal plasma flow significantly in the postobstructed kidney. Angiotensin II also appears to mediate tubular interstitial fibrosis in the obstructed kidney. Indeed, use of angiotensin-converting enzyme inhibitors decreases the degree of interstitial fibrosis and the increased deposition of collagen seen in rats with prolonged ureteral obstruction.