Cardiovascular manifestations of renovascular hypertension in diabetic mice

Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN, United States of America
Wartburg College, Waverly, IA, United States of America
Hannover Medical School, Medizinischen Hochschule Hannover (MHH), Hannover, Germany
Department of Medicine, Chulalongkorn University, Bangkok, Thailand
Division of Nephrology and Hypertension, Mayo Clinic, Rochester, MN, United States of America
DOI
10.7287/peerj.preprints.1323v2
Subject Areas
Cardiology, Diabetes and Endocrinology, Nephrology, Pathology, Translational Medicine
Keywords
renal artery stenosis, cardiovascular disease, Diabetes, hypertension
Copyright
© 2015 Kashyap et al.
Licence
This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, reproduction and adaptation in any medium and for any purpose provided that it is properly attributed. For attribution, the original author(s), title, publication source (PeerJ PrePrints) and either DOI or URL of the article must be cited.
Cite this article
Kashyap S, Engel S, Osman M, Al-Saiegh Y, Wongjarupong A, Grande JP. 2015. Cardiovascular manifestations of renovascular hypertension in diabetic mice. PeerJ PrePrints 3:e1323v2

Abstract

Purpose. Type 2 diabetes is the leading cause of end stage renal disease in the United States. Atherosclerotic renal artery stenosis is commonly observed in diabetic patients and impacts the rate of renal and cardiovascular disease progression. We hypothesized that renal artery stenosis contributes to bilateral renal disease in diabetics. In our original study, we found that leptin-deficient diabetic (db/db) mice subjected to RAS developed severe and bilateral renal disease, with the contralateral (uncuffed) kidney showing features reminiscent of progressive diabetic nephropathy. In non-diabetic mice (WT), the cuffed kidney developed progressive atrophy, but the contralateral kidney showed minimal histopathologic alterations. In doing these studies, we observed increased sudden death in db/db mice with RAS, but not in WT mice with RAS. The objective of this study was to characterize the aortic and cardiac phenotype of db/db mice subjected to RAS. Methods. We developed a murine model of renal artery stenosis by placement of a polytetrafluoroethylene cuff on the right renal artery in db/db mice. We studied 109 WT and 95 db/db mice subjected to Renal artery stenosis (RAS) or sham surgery. Results. The mortality rate of db/db RAS mice was about 23.5%, whereas only 1.5% deaths were observed in WT RAS mice. Interestingly, 60% of mortality in the db/db mice occurred in the first two weeks following RAS surgery. Necropsy showed massive intrathoracic hemorrhage associated with aortic dissection. Aortas from db/db RAS mice showed more smooth muscle dropout, medial disruption, and hemorrhage than aortas from WT mice with RAS. Cardiac tissue from db/db RAS mice had more fibrosis than did cardiac tissue from WT RAS mice. Conclusions. Db/db mice subjected to RAS are prone to develop fatal aortic dissection, which is not observed in WT mice with RAS. The db/db RAS model provides the basis for future studies directed towards defining basic mechanisms underlying the interaction of hypertension and diabetes on the development of aortic lesions.

Author Comment

The title has been changed to reflect cardiac as well as vascular manifestations of diabetic renovascular hypertension. The number of mice evaluated at each time period has been added. New data related to alpha smooth muscle actin expression in aortas has been added.

Supplemental Information

Data used for the figures 2, 3 and 4E

DOI: 10.7287/peerj.preprints.1323v2/supp-1

Raw dataset used for the paper

DOI: 10.7287/peerj.preprints.1323v2/supp-2