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Mechanisms behind myocardial depression in rat renal hypertension
P Friberg1, M Nordlander, H Rupp
1Department of Physiology, University of Gothenburg, Sweden.
Insights
In rat renal hypertension, cardiac function declines due to an unknown agent counteracting hypertrophy. Antihypertensive therapy did not improve maximal cardiac function in this study.
Area of Science:
- Cardiology
- Nephrology
- Physiology
Background:
- Cardiac function is depressed in rat renal hypertension.
- The exact causes of this impairment, such as cardiac hypertrophy and increased collagen, are not fully understood.
Purpose of the Study:
- To investigate the mechanisms behind the deterioration of left ventricular function in rat renal hypertension.
- To examine cardiac function, myocardial morphology, myosin iso-enzymes, plasma renin activity, and high-energy compounds.
Main Methods:
- Studied cardiac function, myocardial morphology, myosin iso-enzymes, plasma renin activity, and high-energy compounds.
- Utilized rats with two-kidney, one-clip renal hypertension and reversed renal hypertension models.
- Compared untreated hypertensive rats with those receiving antihypertensive therapy.
Main Results:
- Maximal cardiac function was not altered by antihypertensive therapy compared to untreated hypertensive rats.
- Alterations in iso-enzyme patterns, plasma renin activity, and myocardial morphology were less significant for cardiac performance.
- Findings suggest a negative inotropic agent counteracts hypertrophy-induced left ventricular enhancement.
Conclusions:
- A circulating negative inotropic agent, of either renal or non-renal origin, is released during two-kidney, one-clip renal hypertension.
- This agent counteracts the positive effects of cardiac hypertrophy on left ventricular performance.
- The precise identity and origin of this agent require further investigation.
Abstract:
Cardiac function in rat renal hypertension has been shown repeatedly to be depressed. The reason for this impairment has not been fully understood, although cardiac hypertrophy and increased collagen content have been claimed as possible causes. To further unravel the mechanisms underlying the deterioration of left ventricular function in rat renal hypertension, we investigated cardiac function, myocardial morphology, myosin iso-enzymes, plasma renin activity and levels of myocardial high-energy compounds in hearts from rats exposed to renal and reversed renal hypertension. Maximal cardiac function was unaltered in hearts exposed to antihypertensive therapy from the time of renal artery clipping compared with untreated hypertensive rats. The observed alterations of iso-enzyme pattern, plasma renin activity levels and myocardial morphology among the groups showed to be of less importance with respect to cardiac performance. Together with previous results from our laboratory, the present findings suggest that some negative inotropic agent of renal or non-renal origin is released during two-kidney, one clip renal hypertension, which counteracts the enhanced left ventricular performance induced by cardiac hypertrophy.