Blockade of the renin-angiotensin-aldosterone system has proved effective i
n retarding the progression of renal disease in the remnant kidney model, a
s well as other experimental diseases, and most importantly, in a range of
progressive human renal diseases. Attention has focused on the role of angi
otensin II in propagating progression both by its hemodynamic and non-hemod
ynamic actions. Recent evidence, predominantly in the remnant kidney model,
indicates that the drugs used to block this hormone system, angiotensin-co
nverting enzyme inhibitors and angiotensin II receptor blockers, also lower
aldosterone levels. Aldosterone as well as angiotensin II thus appears to
be instrumental in sustaining the hypertension and fibroproliferative destr
uction of the residual kidney. Curr Opin Nephrol Hypertens 10:105-110. (C)
2001 Lippincott Williams & Wilkins.