1. The response of systemic and regional haemodynamic indices to increasing infusion rates of angiotensin II (1, 3 or 10 ng min−1 kg−1) or placebo [5% (w/v) d-glucose] was studied in eight normal male subjects.
2. As compared with placebo, angiotensin II infusion caused an incremental rise in the serum angiotensin II level [14.5 ± 7.7 (placebo) to 187.2 ± 36.1 (10 ng of angiotensin II min−1 kg−1) pmol/l; mean ± 95% confidence interval] associated with a stepwise increase in total peripheral resistance [880 ± 42 (placebo) to 1284 ± 58 (10 ng of angiotensin II min−1 kg−1) dyn s cm−5] and a progressive reduction in cardiac output [8.3 ± 0.4 (placebo) to 7.0 ± 0.4 (10 ng of angiotensin II min−1 kg−1) litres/min].
3. A stepwise fall in renal blood flow was observed with increasing angiotensin II infusion rate [1302 ± 65 (placebo) to 913 ± 64 (10 ng of angiotensin II min−1 kg−1) ml/min]. In contrast, calf blood flow was unaffected by 1 ng or 3 ng of angiotensin II min−1 kg−1 and was significantly increased by 10 ng of angiotensin II min−1 kg−1 (P < 0.01).
4. Calf venous capacitance was uninfluenced by 1 ng of angiotensin II min−1 kg−1, but was significantly increased by both 3 ng (P < 0.005) and 10 ng (P < 0.001) of angiotensin II min−1 kg−1.
5. Our results indicate that the pressor response to angiotensin II is a summation of multiple regional haemodynamic effects which differ qualitatively not only with the vascular bed studied but also within a single tissue, with the level of circulating angiotensin II attained.
6. The venodilatation we have demonstrated with high angiotensin II levels may effect a potentially favourable redistribution of blood flow in situations of inappropriate extracellular fluid volume expansion, such as chronic heart failure.