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(Hypertension. 1995;26:321-326.)
© 1995 American Heart Association, Inc.
Articles |
From the Institute of Medicina Clinica, Cattinara Hospital, University of Trieste, and Cattedra di Medicina Interna, University of Brescia (M. Castellano) (Italy).
Correspondence to Bruno Fabris, MD, Università di Trieste, Istituto di Medicina Clinica, c/o Ospedale di Cattinara, 34149 Trieste, Italy.
Abstract Left ventricular hypertrophy with diffuse intermyocardiocytic fibrosis is a feature of uremia. The role of blood pressure and/or other cardiovascular uremic risk factors in cardiac remodeling is still uncertain. To determine the extent to which improvement of kidney function and the control of uremia-related risk factors are associated with a reduction of myocardial injury, we evaluated the effect of dietary protein restriction or the angiotensin-converting enzyme inhibitor lisinopril on cardiac structure in remnant kidney rats. One week after subtotal nephrectomy, Wistar rats were allocated to receive drinking water solution (group 1), 5 mg/kg per day lisinopril (group 2), or a low-protein diet (6%) (group 3) for 12 weeks. Groups 2 and 3 showed a comparable efficacy in preventing the expected rise in creatininemia, urinary protein excretion, and glomerulosclerosis. However, hypertension development was prevented only in group 2. Groups 1 and 3 developed a significant (P<.01) increase in left ventricular weight (2.45±0.1 and 2.5±0.5 mg/g body wt, respectively) compared with group 2 (1.9±0.06 mg/g body wt). Cardiac hydroxyproline concentration was also lower in group 2 compared with group 1 (2.07±0.16 versus 2.73±0.17 mg/g left ventricular weight, P<.05) but not compared with group 3 (2.59±0.19 mg/g left ventricular weight). The effect of angiotensin-converting enzyme inhibition on left ventricular mass and intracardiac collagen content appeared to be dissociated from anemia, sympathetic activity, and hyperlipidemia. There was a close relationship between systolic pressure and left ventricular mass; however, no relationship between the degree of cardiac fibrosis and systolic pressure could be determined. Compared with other uremia-related risk factors, control of systemic blood pressure is an essential component of the prevention of left ventricular hypertrophy, and the limitation of interstitial fibrosis may occur by a mechanism other than blood pressure control.
Key Words: hypertension, experimental uremia hypertrophy fibrosis angiotensin-converting enzyme inhibitors
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