Weinberger H D, Martin B A, Gattone V H, Evan A P, Connors B A, Luft F C, Willis L R
J Submicrosc Cytol. 1986 Jan;18(1):29-34.
We have observed alterations of glomerular and afferent arteriolar structure in nephrotoxic and ischemic models of acute renal failure. These alterations may have been caused by angiotensin II. To test this notion, we infused the peptide directly into the left renal artery of anesthetized rats. At sub-pressor doses of 1.9 and 6.5 ng/100g body weight/min, the peptide caused dose-related decreases in glomerular filtration rate similar to those that occur in models of acute renal failure. In some animals, methacrylate casts of the infused and contralateral kidneys were made for later examination by scanning electron microscopy. In other animals, the kidneys were fixed with glutaraldehyde for examination of the glomerular epithelium and endothelium by scanning electron microscopy. Cast analysis showed no detectable alteration of afferent arteriolar diameter, and only moderate bilateral changes in the tapering of the arterioles. In contrast, the diameter of the casted glomerular tuft was significantly reduced by the highest dose of angiotensin II. No alterations of the glomerular epithelium or endothelial fenestrae were observed. We conclude that angiotensin II probably did not mediate the changes in glomerular structure in our earlier studies of acute renal failure, even though similar reductions of glomerular filtration rate occurred. Reduced diameter of the glomerular tuft is consistent with a possible role for angiotensin II as a modulator of intrinsic contractile elements in glomeruli.
