Related Experiment Videos
Contribution of systemic blood pressure to myocardial remodeling in uremic rats
B Fabris1, R Carretta, F Fischetti
1Institute of Medicina Clinica, Cattinara Hospital, University of Trieste, Italy.
Insights
Dietary protein restriction and lisinopril helped manage kidney disease markers in rats. However, only lisinopril prevented hypertension and reduced cardiac fibrosis, suggesting its benefit for uremic cardiomyopathy.
Area of Science:
- Nephrology
- Cardiology
- Uremic Cardiomyopathy
Background:
- Uremia is associated with left ventricular hypertrophy and fibrosis.
- The impact of uremic risk factors on cardiac remodeling remains unclear.
Purpose of the Study:
- To investigate how improved kidney function and controlled uremic risk factors affect myocardial injury.
- To evaluate the effects of dietary protein restriction and lisinopril on cardiac structure in remnant kidney rats.
Main Methods:
- Wistar rats underwent subtotal nephrectomy.
- Groups received either a control solution, lisinopril (5 mg/kg/day), or a low-protein diet (6%) for 12 weeks.
- Evaluated creatininemia, urinary protein, glomerulosclerosis, blood pressure, left ventricular weight, and cardiac hydroxyproline concentration.
Main Results:
- Both lisinopril and low-protein diet reduced kidney disease markers.
- Hypertension was prevented only by lisinopril.
- Lisinopril significantly reduced left ventricular weight and cardiac fibrosis compared to controls.
- Low-protein diet did not significantly reduce cardiac fibrosis compared to controls.
Conclusions:
- Angiotensin-converting enzyme inhibition with lisinopril effectively reduces cardiac remodeling in uremic rats, independent of anemia or hyperlipidemia.
- Blood pressure control is crucial in mitigating uremic cardiomyopathy.
- Dietary protein restriction alone may not be sufficient to prevent cardiac fibrosis in uremia.
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. Group 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 hydroxyporline 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.(ABSTRACT TRUNCATED AT 250 WORDS)