Left ventricular hypertrophy in rats with renovascular hypertension. Alterations in cardiac function and adrenergic responses.

Performance of the hypertrophied left ventricle was studied by determination of the inotropic response to different stimuli in renal hypertensive rats (two-kidney, one clip Goldblatt, RHR, n = 13) and matched sham-operated controls (NR, n = 11). A model was developed to determine maximal pressure development (transient aortic ligation), maximal pumping ability (rapid transfusion, 2 ml/30 sec), and responses to beta stimulation (isoproterenol, 0.01 to 0.10 micron g/kg/min), using dP/dt/P40 as a load-independent index of contractility. With rapid blood transfusion, RHR developed a higher ventricular systolic pressure (211.5 +/- 10.1 mm Hg vs 194.0 +/- 9.3 (SE), p less than 0.001) but at the expense of higher end-diastolic pressure (LVEDP) (12.2 +/- 1.1 mm Hg vs 7.7 +/- 1.0, p less than 0.02). The maximal response of dP/dt/P40 to isoproterenol was diminished in RHR (29.5 +/- 3.2 sec-1 vs 49.6 +/- 5.2, p less than 0.01) whereas the maximal developed pressure (MDP) was greater in RHR than in NR (239.2 +/- 7.5 mm Hg vs 197.0 +/- 3.9, p les than 0.001). A positive correlation was found between MDP and ventricular weight (r = 0.846, p less than 0.001) in contrast with the negative correlation found between ventricular weight and maximal dP/dt/P40 response to isoproterenol (r = 0.677, p less than 0.001). Thus, cardiac hypertrophy in RHR allowed higher developed ventricular pressures but at the expense of higher LVEDP; at the same time, however, the ability to increase contractility in response to beta adrenergic stimulation was decreased. The contrast in results obtained using different tests of cardiac function indicates the need for a multifactorial approach. It also suggests a subtle transformation in this hypertrophy of the pattern of cardiac adaptation to the increased load.