This study examined the ability of [des-Asp1]angiotensin II (angiotensin III, ANG III) to interact with the angiotensin II (ANG II) receptors involved in pressor hyperresponsiveness in one-kidney, 3-day renal artery stenosis (RAS) rabbits. In experiment 1, six 3-day RAS rabbits had significantly larger pressor responses to norepinephrine (NE; 800 ng.min-1.kg body wt-1) than did six 3-day controls. The intravenous infusion of captopril, an angiotensin-converting enzyme inhibitor, diminished the pressor response NE in the RAS rabbits. ANG III at 0.5, 1.0, and 2.0 pmol.min-1.kg-1 iv with captopril resulted in a progressive restoration of pressor hyperresponsiveness to NE in the RAS rabbits, and ANG II at 2.0 pmol.min-1.kg-1 iv produced no further enhancement of the pressor responses to NE. In experiment 2, 12 3-day RAS rabbits had pressor hyperresponsiveness to NE that was alleviated by the infusion of captopril and was restored by the intravenous infusion of ANG III (2 pmol.min-1.kg-1). In six of the these rabbits an additional intravenous infusion of the ANG II antagonist [Sar1,Ile8]ANG II at 300 ng.min-1.kg body wt-1 diminished the pressor hyperresponsiveness to NE; in the other six rabbits the infusion of [Sar1,Ala8] ANG II at 6 micrograms.min-1.kg body wt-1 did not reduce the pressor hyperresponse to NE. In experiment 3, the infusion of ANG III (5 pmol.min-1.kg-1) in six normal rabbits did not alter the pressor responses to NE (400 ng.min-1.kg-1), whereas the infusion of ANG II (5 pmol.min-1.kg-1) resulted in increased pressor responses to NE.(ABSTRACT TRUNCATED AT 250 WORDS)