Aberrant Renal Vascular Morphology and Renin Expression in Mutant Mice Lacking Angiotensin-Converting Enzyme by Karl F. Hilgers, Vasantha Reddi, John H.

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Aberrant Renal Vascular Morphology and Renin Expression in Mutant Mice Lacking Angiotensin-Converting Enzyme by Karl F. Hilgers, Vasantha Reddi, John H. Krege, Oliver Smithies, and R. Ariel Gomez Hypertension Volume 29(1):216-221 January 1, 1997 Copyright © American Heart Association, Inc. All rights reserved.

Fig 1. Fig 1. Renal morphology and renin distribution in Ace −/− and wild-type mice. Immunoperoxidase staining for renin and hematoxylin counterstain. A, Section from an Ace +/+ wild-type mouse showing immunostaining for renin restricted to the juxtaglomerular area (arrow) and the absence of renin staining in the small arteriole on the left side (arrowhead). Magnification ×208. B, Section from an Ace −/− mouse showing dilated Bowman’s spaces (asterisk), tubular atrophy (arrow), and interstitial fibrosis (arrowhead). Cells staining strongly positive for renin surround the arterioles, and there is general, although less, renin staining of tubular cells. Magnification ×208. C, Widened, thickened, hypercellular cortical arteriole in Ace −/− kidney (arrow). Individual cells staining strongly for renin are present in the stalk of the adjacent glomerulus and the perivascular interstitium (arrowheads) but not in the smooth muscle layer of the arteriole. Magnification ×417. D, Renin-positive cells in the interstitium of Ace −/− kidney. Magnification ×500. Karl F. Hilgers et al. Hypertension. 1997;29:216-221 Copyright © American Heart Association, Inc. All rights reserved.

Fig 2. Fig 2. Segment of microdissected renal arterial vascular trees from wild-type (left) and Ace −/− mice (right). Both trees were stained for renin (immunoperoxidase technique); magnification ×42. Ace −/− terminal arterioles appear sparse and are widened and thickened compared with the delicate afferent arterioles in the wild-type mice. Note that renin staining is restricted to the end of afferent arterioles in the wild-type vessels (arrows) but that patches of renin staining are present throughout the vascular tree in the Ace −/− (arrowheads). Karl F. Hilgers et al. Hypertension. 1997;29:216-221 Copyright © American Heart Association, Inc. All rights reserved.

Fig 3. Fig 3. Dot blot showing hybridization of serial dilutions of kidney RNA from two Ace −/− mice (ACE −/−) and three wild-type mice (ACE +/+) with radiolabeled mouse renin cDNA. Note that the lowest amount of Ace −/− RNA yields a more intense signal than the highest amount of Ace +/+ RNA. Karl F. Hilgers et al. Hypertension. 1997;29:216-221 Copyright © American Heart Association, Inc. All rights reserved.

Fig 4. Fig 4. Northern blot showing hybridization of 10 μg renal RNA per lane with radiolabeled cDNAs for renin (top), transforming growth factor-β (TGF-β, middle) and GAPDH (bottom). The transcript size in kilobases (kB) is indicated on the right side. Karl F. Hilgers et al. Hypertension. 1997;29:216-221 Copyright © American Heart Association, Inc. All rights reserved.