The effects of ANG II on the efficiency of autoregulatory changes in afferent arteriolar diameter (AAD; n=7, Sprague Dawley rats) in response to alterations of renal arterial pressure were evaluated using experimental studies and control theory. Using the in-vitro blood perfused juxtamedullary preparation and videomicroscopy, AAD responses to changes in perfusion pressure from 60 to 160mmHg were measured with an image shearing monitor. Renal tissue was exposed to ANG II (1nM) and the AT1 receptor antagonist candesarten (CV: 1μM ). ANG II treatment reduced AAD (-9.5±0.41%) and elicited a parallel downshift in the pressure-diameter curve [d(p)] from control (Δslope.-0.23 ±.08% to -0.26±.04%) between 60 and 120 mmHg. Between 140 and 160mmHg that parallel downshift was slightly attenuated. The downshift was modeled as an increase in feedback gain of the controlled variable (AAD) and the attenuation as a loss of the forced response (FR;immediate id(p)) component of stability. The steady state error (SSE) is the post-transient fluctuation (natural response;NR) and is a measure of how effectively the vessel can hold that FR diameter. The ANG II superfused vessels exhibited a significant loss in NR stability (SSE = 1.58 +.49% to 3.76±.5%) but FR stability was lost only in the upper autoregulatory range. CV treatment in the presence of ANG II returned these stability components towards control levels. Imposing feedback gain and SSE on the control model equivalent to those seen experimentally rendered analogous control marginal stability. We conclude that ANG II augments afferent arteriolar control efficiency by destabilizing autoregulation and CV effectively reestablishes autoregulatory efficiency by restoring forced and natural stability.