Angiotensin II and its C-terminal heptapeptide fragment, [des-Asp1]angiotensin II, influence a variety of angiotensin receptors in a qualitatively similar manner. On the basis of potency studies, angiotensin II appears to be the important mediator of the renin-angiotensin system at the peripheral arteriolar receptors to maintain arterial blood pressure. However, both angiotensin II and the heptapeptide are approximately equally potent at receptor sites in the adrenal cortex, the renal arterioles, and the juxtaglomerular cells of the kidneys. Adrenal cortical receptor affinity appears to be greater for the heptapeptide than for angiotensin II. Analogues of the heptapeptide are better antagonists than analogues of the octapeptide in blocking the steroidogenic responses to both angiotensin II and heptapeptide. Circulating plasma levels of [des-Asp1]angiotensin II appear to be low in most species; there is strong evidence, however, that local generation of heptapeptide can occur under certain conditions. It seems likely that both peptides act at common receptor sites to mediate the response to the renin-angiotensin system but more data are needed before a definite physiologic role can be assigned to the heptapeptide.