The development of an increased ventricular wall mass was followed from birth until five weeks of age and also later in life in spontaneously hypertensive rats (SHR) which were compared with normotensive control rats (NCR). It was shown that the first signs of enhanced ventricular growth were already evident in SHR in the first week of life. At 10 months of age left ventricular weight was 68% higher in SHR than in matched NCR, at a mean pressure difference of 30%. Treatment of SHR with antihypertensive agents, like hydralazine, hydralazine-guanethidine, propranolol, or metoprolol, from three weeks up to 10 months of age reduced this gross increase in left ventricular weight by only about 10% while the mean pressure difference between SHR and NCR was reduced by 50 to 70%. It appears that the increase in left ventricular wall mass in SHR is initiated so early in life and is of such a character that it can only, to a fairly minor extent, be reversed or prevented by pressure-lowering procedures. Part of the explanation may be a substantial contribution of myocardial hyperplasia, in association with a genetically linked predisposal to structural cardiovascular adaptation, either 'inherent' in the effectors and/or caused by 'trophic' influences of a hormonal and/or transmitter nature.