In the rat, experimental renal vasoconstriction induced by the use of a Goldblatt clamp caused arterial hypertension, cardiomyocyte hypertrophy and an increased capillary to cardiomyocyte ratio, the latter indicating the formation of new cardiac capillaries. Total capillary density decreased, but capillary portions expressing alkaline phosphatase increased. This suggested a greater arterialization of capillaries which would increase the flow of arterial blood to the myocardial capillary nets. However, the observed increase in the area of the capillary domains means the extra arterialization was not sufficient to compensate for the lengthening of the oxygen diffusion pathway caused by the hypertrophy. Since the effects of renal vasoconstriction were not seen in rats treated with an inhibitor of angiotensin converting enzyme (ACE) it is suggested they are induced by angiotensin II via activation of the renin-angiotensin system (RAS).