Cardiovascular hypertrophy in spontaneously hypertensive rats.

In 1974 we reported that left ventricular mass correlated poorly with blood pressure levels during both the development and the reversal of hypertensive cardiac hypertrophy. This study, which was confirmed by many, has since been extended along two main lines: investigation of the factors modulating left ventricular hypertrophy and of associated changes in contractile protein, and comparison of the left ventricular structural response to hypertension with those of the large and small resistance vessels. In addition to blood pressure control, two factors were identified as important modulators of left ventricular hypertrophy: the level of cardioadrenergic activity and a recently isolated myocardial factor in SHR which stimulates in vitro cardiac protein synthesis. Of greater importance haemodynamically are the structural changes in the small resistance vessels; these were estimated from resistance to constant flow during maximal vasodilatation (Folkow). Captopril-hydrochlorothiazide led to a significantly greater reduction in that index than hydralazine, although both led to equal blood pressure control. Despite some general parallelism, the structural cardiovascular responses to hypertension were not homogeneous; important differences were found among the heart, aorta and resistance vessels. The development and regression of cardiovascular hypertrophy are not dependent on mechanical load alone but seem to be modulated at three levels - increased pressure load, level of cardioadrenergic activity and local growth factor.