The present study has developed a new hypothesis for the regulation of renal hemodynamics based on the theory of a metabolic control of local blood flow. Adenosine has been proposed as the mediator of tubuloglomerular feedback. We have reported on the renal effects of adenosine, the renal tissue levels of adenosine in relation to those of ATP, and the effects of adenosine synergistic substances (dipyridamole, erythrohydroxynonyladenine) and adenosine antagonistic substances (theophylline, adenosine deaminase) on the tubuloglomerular feedback response of the nephron. A hypothetic model has been presented that incorporates adenosine as a mediator in the signal transmission of the tubuloglomerular feedback mechanism.