|
|
||||||||
CARDIAC, RENAL, AND RESPIRATORY INTEGRATION
1Laboratory of Biochemistry, Bicêtre Hospital, 94270 Le Kremlin-Bicêtre; 2Institut National de la Santé et de la Recherche Médicale U 430, Broussais Hospital, 75014 Paris and Claude Bernard Association, 75005 Paris; 3Laboratory of Biochemistry, Charles Foix Hospital, 94205 Ivry sur Seine; and 4Laboratory of Applied Biochemistry, Faculty of Pharmaceutical and Biological Sciences, 92296 Châtenay-Malabry, France
Submitted 28 August 2002 ; accepted in final form 3 December 2003
Chronic renal failure often induces left ventricular hypertrophy. We assessed whether the heart is affected in the Zucker obese rat, a model of chronic renal failure associated with obesity, glucose intolerance, and insulin resistance without hypertension or hyperglycemia. After systemic blood pressure measurement, the heart, the aorta, and the kidneys were removed from anesthetized 9- and 13-mo-old Zucker obese and lean control male rats (n = 33, n = 24, n = 25, and n = 21, respectively). Determination of left ventricular geometry, quantification of myocardium collagen density, and measurement of heart antioxidant enzyme activity were made, as well as aorta and kidney parameters. Mean blood pressure remained at a normal range whatever the age and group considered. Whereas kidney structure and function were severely impaired, no sign of myocardial infarction or inflammatory process was noticed. A moderate left ventricular hypertrophy was observed in 13-mo-old obese rats. While heart malondialdehyde was stable with age and among groups, antioxidant enzyme activity was higher in obese rats. In conclusion, in the absence of hypertensive or hyperglycemic disorders, the heart seems to display a sufficient line of defense against oxidative stress during the development of cardiac hypertrophy.
left ventricular hypertrophy; renal failure; oxidative stress; Zucker rats; hyperlipidemia
This article has been cited by other articles:
![]() |
J. Allard, M. Buleon, E. Cellier, I. Renaud, C. Pecher, F. Praddaude, M. Conti, I. Tack, and J.-P. Girolami ACE inhibitor reduces growth factor receptor expression and signaling but also albuminuria through B2-kinin glomerular receptor activation in diabetic rats Am J Physiol Renal Physiol, October 1, 2007; 293(4): F1083 - F1092. [Abstract] [Full Text] [PDF] |
||||
![]() |
A. Guellich, T. Damy, Y. Lecarpentier, M. Conti, V. Claes, J.-L. Samuel, J. Quillard, J.-L. Hebert, T. Pineau, and C. Coirault Role of oxidative stress in cardiac dysfunction of PPAR{alpha}-/- mice Am J Physiol Heart Circ Physiol, July 1, 2007; 293(1): H93 - H102. [Abstract] [Full Text] [PDF] |
||||
![]() |
S. Boudina and E. D. Abel Diabetic Cardiomyopathy Revisited Circulation, June 26, 2007; 115(25): 3213 - 3223. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. F. Carroll, W. J. Zenebe, and T. B. Strange Cardiovascular Function in a Rat Model of Diet-Induced Obesity Hypertension, July 1, 2006; 48(1): 65 - 72. [Abstract] [Full Text] [PDF] |
||||
![]() |
I. G. Poornima, P. Parikh, and R. P. Shannon Diabetic Cardiomyopathy: The Search for a Unifying Hypothesis Circ. Res., March 17, 2006; 98(5): 596 - 605. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |