The relationship between tubuloglomerular feedback (TGF) and SNGFR autoregulation has been analyzed, and the results show that renal autoregulation is much more complex than a single feedback-loop control system that regulates SNGFR or renal blood flow. At least two mechanisms seem to be involved. First, there appears to be a TGF-independent component in autoregulation that is probably myogenic in nature, located in the renal vasculature, and responsive to changes in intravascular pressure or transmural pressure difference. The second mechanism is TGF, which involves both vascular and tubular elements, responds to changes in either SNGFR or proximal nephron reabsorption, and acts in concert with glomerulotubular balance (GTB) to stabilize distal delivery of tubular fluid. In a strict sense, neither SNGFR nor renal blood flow are "controlled" during autoregulation. The stabilization of these important variables is an intermediate result of the action of the control mechanisms to directly regulate other system variables. Moreover, because both TGF and GTB are influenced by changes in extracellular volume (ECV), autoregulation is an adaptive control mechanism. Thus, in autoregulation, TGF acts to ensure a balance between filtration and proximal and loop of Henle reabsorption that is appropriate for the prevailing ECV status of the animal.