Abnormal polyamine metabolism in hypertensive cardiac hypertrophy
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Published on: June 14, 2016
M Shimizu1, I Masuda, K Aihara
1Third Department of Internal Medicine, Jikei University School of Medicine, Tokyo, Japan.
Insights
This study investigated hypertensive cardiac hypertrophy in rats using polyamine levels. Captopril suppressed cardiac hypertrophy, while diltiazem did not, indicating its inhibitory effect.
Area of Science:
- Cardiology
- Pharmacology
- Biochemistry
Background:
- Hypertensive cardiac hypertrophy is a significant clinical concern.
- Polyamines, such as spermidine, play a role in cellular growth and hypertrophy.
- Understanding the impact of antihypertensive agents on cardiac hypertrophy is crucial.
Purpose of the Study:
- To assess myocardial hypertrophic activity in spontaneously hypertensive rats (SHR) and Wistar Kyoto (WKY) rats.
- To evaluate the effects of diltiazem, hydralazine, and captopril on hypertensive cardiac hypertrophy.
- To determine if myocardial polyamine concentrations can serve as indicators of hypertrophic activity.
Main Methods:
- Analysis of myocardial polyamine concentrations in SHR and WKY rats.
- Administration of diltiazem, hydralazine, and captopril to SHR rats for 5 weeks.
- Measurement of blood pressure, heart weight, and spermidine concentration.
Main Results:
- SHR rats exhibited elevated blood pressure, enlarged hearts, and higher myocardial spermidine compared to WKY rats.
- Diltiazem treatment lowered blood pressure but did not prevent increases in heart weight or spermidine.
- Hydralazine suppressed blood pressure and spermidine increases but not heart weight increase.
- Captopril suppressed increases in blood pressure, heart weight, and spermidine concentration.
Conclusions:
- Spermidine concentration is a sensitive indicator of cardiac hypertrophic activity.
- Captopril effectively inhibits hypertensive cardiac hypertrophy.
- Diltiazem does not inhibit cardiac hypertrophy, and hydralazine may lead to earlier plateauing of hypertrophy.
Abstract:
In order to assess myocardial hypertrophic activity during the process of hypertensive cardiac hypertrophy in the presence and absence of treatment with anti-hypertensive agents, we analyzed myocardial polyamine concentrations in spontaneous hypertensive (SHR) rats and control rats of Wistar Kyoto (WKY) strain. The anti-hypertensive agents studied were diltiazem, hydralazine and captopril, each of which was administered for 5 weeks. In comparison with WKY rats, SHR rats showed elevated blood pressure and enlarged hearts with higher myocardial spermidine concentration. Although blood pressure was lowered in the diltiazem-treated SHR rats, heart weight and myocardial spermidine concentration increased as in untreated SHR rats. In the hydralazine-treated group increases in both blood pressure and myocardial spermidine concentration were suppressed, while an increase in heart weight was not. In the captopril-treated group, increases in blood pressure, heart weight and spermidine concentration were all suppressed. Since spermidine level appears to be a sensitive indicator of hypertrophic activity in the heart, this study suggests that captopril exerts an inhibitory effect on hypertensive cardiac hypertrophy whereas diltiazem does not. It also suggests that hypertrophy may reach a certain plateau level earlier in the hydralazine-treated animals than in others.
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