Regression of left ventricular hypertrophy and prevention of left ventricular dysfunction by captopril in the spontaneously hypertensive rat.

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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-mo.-old female SHR and normotensive American Wistar rats (NWR) were treated for 10 mo. with an inhibitor of angiotensin I-converting enzyme, captopril (2 g/l of drinking water). Captopril reduced the marked left ventricular hypertrophy of 24-mo.-old SHR (untreated 4.37 .+-. 0.2 mg/g body wt; treated, 3.01 .+-. 0.1 mg/g; P < 0.02) to levels observed in 6-mo.-old SHR. Treatment prevented the reductions in baseline and maximal aortic blood flows that occurred in SHR between ages 12-24 mo. 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-mo.-old untreated NWR, 84 .+-. 3%; untreated SHR, 56 .+-. 5%; P < 0.001). Therapy restored this index in SHR to normal (77 .+-. 4%). The relationship between ejection-fraction index and afterload was also normal in treated SHR. Chronic therapy with captopril produced a marked regression of cardiac hypertrophy and prevented the deterioration of cardiac performance in SHR with long-standing hypertension.