Cardiac performance in rats with renal hypertension.

Abstract

SUMMARY To evaluate cardiac performance in renal hypertension more precisely we determined cardiac function curves for 12 normotensive rats and 11 other rats with two-kidney Goldblatt hypertension. The hypertensive group (BP = 134 ± 8 mm Hg) showed significant cardiac hypertrophy (44 ± 1% increased ratio of heart weight to body weight, P < 0.01) and markedly increased left ventricular stroke work with a moderate but not significant increase in left ventricular end-diastolic pressure (LVEDP) (5.9 ± 0.8 vs. CARDIAC hypertrophy generally has been considered one of the principal long-term mechanisms of compensation for cardiac stress; 1 the increase in cardiac mass is believed to make the heart as strong a pump as it had been previously. It is known that the increase in contractile strength which follows hypertrophy is due to an increase in muscle mass and that the strength of individual muscle fibers remains unchanged or even may decrease slightly. 2 ' 7 The influence of myocardial hypertrophy on the performance of the hypertensive heart is of particular interest because cardii.c hypertrophy frequently accompanies arterial hypertension and it has been pointed out that early hypertension, in both man and animals, is associated with an increased cardiac output and signs of a hyperkinetic circulation. 8 " 11 The relationship of the increased cardiac output to the development of cardiac hypertrophy has yet to be investigated. Recent studies which show an increased cardiac contractility during the onset of renal hypertension 12 and the early development of cardiac hypertrophy in two forms of hypertension 13 -14 suggest a causal relationship between increased cardiac output and development of cardiac hypertrophy.With the advent of refinements in microtransducer technology it has become possible to accurately measure cardiac output and arterial and venous pressures in small mammals with and without arterial hypertension and thus evaluate cardiac performance in a precise manner. Further, correlation of hemodynamic alterations with biochemical changes which characterize the type of hypertrophy should open the way for a better understanding of cardiac mechanics. To our knowledge this has not been attempted before in hypertensive heart disease, nor is there direct information on the effects of cardiac hypertrophy on ventricular function curves (see Reference 15 for review). We therefore studied the functional link between the appearance of cardiac hypertrophy and the performance of the heart in rats with chronic renal hypertension. MethodsWe performed experiments on 20 normal Wistar rats and on 14 rats with sustained renal hypertension (average duration, 9 weeks; range, 6-22 weeks). All data presented are expressed as mean ± SE, unless stated otherwise for a specific value.Hypertension was produced by placing a silver clip with a 0.20-mm gap around the left renal artery; the contralateral kidney was left untouched. The rats were 10 weeks old at the time of constriction and average weight was 244 ± 11 g. All rats were housed...

Angiotensin and the remodelling of the myocardium.

“…This same perivascular and streaky fibrosis was found in the rat myocardium following systemic microsphere embolization and the appearance of sclerotic glomeruli (Carroll et al, 1989). The collagen concentration of the myocardium in renovascular hypertension, as measured by either its concentration of hydroxyproline or its morphometrically determined collagen volume fraction, is elevated (Averill et al, 1976;Bartosova etal., 1969;Doering etal., 1988;Jalil et al, 1988;Michel et al, 1986b;Sen & Bumpus, 1979;Thiedemann etal., 1983;Weber et al, 1988b). Thus, there is little question that collagen accumulation and its structural remodelling are an integral component of the pressure overload state that accompanies renovascular hypertension and which, in some yet undefined manner, may be related to elevated circulating angiotensin II.…”

Hydrochlorothiazide improves ventricular compliance and thus performance without reducing hypertrophy in renal artery stenosis in rats.

“…26 The 2K1C rat model, however, has been shown to develop early changes in cardiac performance. 6 In our experiment, we were able to show a right shift of the cardiac function curve in 2K1C rats as assessed by measuring cardiac output and stroke volume at different filling pressures. This finding is consistent with what has previously been demonstrated.…”

“…This finding is consistent with what has previously been demonstrated. 6 This change is unlikely to be as a result of differences in afterload measured during the cardiac performance experiment, or differences in heart weight, because a similar change in the stroke work (expressed per gram of heart weight)-filling pressure relation was also found. The explanation for a decreased cardiac function at different filling pressures in 2K1C rats is an altered ventricular compliance.…”

Cardiac conditioning ameliorates cardiac dysfunction associated with renal hypertension in rats.

“…However, in rats this is generally associated with depressed myocardial contractility and ventricular function (4)(5)(6)(7). On the other hand, hypertrophy associated with hyperthyroidism or with physical training has frequently been found to be associated with enhanced myocardial contractile performance and ventricular function (8).…”