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Regression of left ventricular hypertrophy and prevention of left ventricular dysfunction by captopril in the
Insights
Chronic captopril therapy significantly reversed cardiac hypertrophy and improved cardiac performance in spontaneously hypertensive rats (SHR). This antihypertensive treatment prevented heart function decline in rats with long-term hypertension.
Area of Science:
- Cardiovascular Physiology
- Pharmacology
Background:
- Long-term hypertension in spontaneously hypertensive rats (SHR) leads to cardiac hypertrophy and impaired cardiac performance.
- Understanding the effects of antihypertensive therapy on established cardiac changes is crucial.
Purpose of the Study:
- To investigate if chronic antihypertensive therapy with captopril can prevent or reverse cardiac hypertrophy and cardiac performance deterioration in SHR.
- To assess the impact of captopril on cardiac function parameters in long-term hypertensive rats.
Main Methods:
- Female SHR and normotensive Wistar rats (NWR) were treated for 10 months with captopril (an angiotensin I-converting enzyme inhibitor).
- Cardiac hypertrophy was quantified by measuring left ventricular mass relative to body weight.
- Cardiac performance was evaluated by assessing aortic blood flow, stroke volume, and ejection fraction index under varying afterload conditions.
Main Results:
- Captopril treatment significantly reduced left ventricular hypertrophy in SHR, bringing it to levels seen in younger SHR.
- Therapy prevented the decline in baseline and maximal aortic blood flows observed in untreated SHR.
- Captopril normalized the reduced ejection-fraction index and the relationship between ejection fraction and afterload in treated SHR.
Conclusions:
- Chronic captopril therapy effectively induced regression of cardiac hypertrophy in SHR.
- Antihypertensive treatment with captopril prevented the deterioration of cardiac performance associated with long-standing hypertension in this rat model.
Abstract:
To determine whether chronic antihypertensive therapy prevents the progression of cardiac hypertrophy and the deterioration in cardiac performance observed in spontaneously hypertensive rats (SHR) with long-term hypertension, 14-month-old female SHR and normotensive American Wistar rats (NWR) were treated for 10 months with an inhibitor of angiotensin I-converting enzyme, captopril (2 g/liter of drinking water). Captopril reduced the marked left ventricular hypertrophy of 24-month-old SHR (untreated, 4.37 +/- 0.2 mg/g of body weight; treated, 3.01 +/- 0.1 mg/g; P less than 0.02) to levels observed in 6-month-old SHR. Treatment prevented the reductions in baseline and maximal aortic blood flows that occurred in SHR between ages 12 and 24 months yet had no effect on the blood flows of NWR. The diminished maximal stroke volume of untreated SHR was ejected from a significantly increased left ventricular end-diastolic volume, so that the ejection-fraction index was markedly reduced (24-month-old untreated NWR, 84 +/- 3%; untreated SHR, 56 +/- 5%; P less than 0.001). Therapy restores this index in SHR to normal (77 +/- 4%). The relationship between ejection-fraction index, and afterload was also normal in treated SHR. Thus, chronic therapy with captopril produced a marked regression of cardiac hypertrophy and prevented the deterioration of cardiac performance in SHR with long-standing hypertension.