Over the past several years, a growing body of information has confirmed and extended our initial concept that nonhemodynamic as well as hemodynamic factors are responsible for the development of left ventricular hypertrophy in hypertension. We reported the dissociation of these factors in the regression of left ventricular mass and hypertrophy with antihypertensive therapy. Several lines of clinical and experimental studies have been pursued to determine whether cardiac performance, myocardial contractility, and reserve are normal with regression of ventricular mass with treatment. Too few studies have been conducted in vivo, and in the conscious state, and at pretreatment pressures to conclude at this time that normal cardiac function and performance is restored or maintained. Until such data are available, we must conclude that although left ventricular hypertrophy confers a risk, in and of itself, to cardiovascular morbidity and mortality, we do not know whether pharmacologic reversal of cardiac hypertrophy is a desirable therapeutic goal. Several years ago we were convinced that a new and impressive body of information emanating mostly from our laboratories strongly indicated a new concept previously unexpressed by others. We suggested that increasing ventricular mass in hypertension (i.e., left ventricular hypertrophy), although dependent in part on arterial pressure and other hemodynamic factors, was also dependent on participation of a number of "nonhemodynamic" mechanisms. Our early findings, supported by associated reports, suggested that in addition to left ventricular afterload, factors including other pressor mechanisms (e.g., adrenergic function and norepinephrine levels, humoral substances, the renopressor system), aging, race, gender, coexisting diseases, pharmacologic agents, and others may also participate.(ABSTRACT TRUNCATED AT 250 WORDS)