The development and reversal of cardiac hypertrophy in hypertension were found not to depend on variations in blood pressure levels alone. There was a marked discrepancy between equipotent antihypertensive drugs in their ability to reverse established hypertrophy; this could be related to differences in reflex sympathetic cardiac stimulation but it also seemed to parallel variations in plasma renin activity. Both AII and (Sar1, Ile8) AII stimulated myocardial protein synthesis and the latter produced cardiac hypertrophy with no significant change in BP. Studies with different neural blockers, AII analogs and combination of drugs as well as in adrenalectomized rats, are planned to evaluate the relative importance of humoral and neurogenic factors that influence cardiac hypertrophy. Determination of myocardial composition has revealed marked differences in changes induced by various antihypertensive drugs but all led to increased hydroxyproline concentration. Cardiac function studies have shown the importance of increased cardiac connective tissue in determining ventricular compliance and cardiac performance. Correlation of hemodynamic studies with biochemical alterations in myocardium will allow better understanding of the alteration in cardiac function in hypertension, of the hemodynamic impact of hypertrophy and of the effects of its treatment. Investigations during the last year have advanced along two lines: (a) continued myocardial studies to determine rate of protein synthesis and the influence of age and increased arterial pressure; in addition further insight was sought regarding the role of renin-angiotensive system in development of hypertrophy. (b) hemodynamic investigations including cardiac function curves in renal hypertensive rats with biochemical composition of myocardium.