Adenosine, a direct degradative product of 5′ AMP, could be a physiological regulator of glomerular filtration rate and renal blood flow, acting on the renal arteriolar tone and the tubuloglomerular feedback mechanism. Recent experimental evidence strongly suggests an important role for intrarenal adenosine in the hemodynamic renal changes observed in postocclusive acute renal failure, in hypoxemia-induced renal insufficiency, as well as in various experimental models of acute renal failure. In these conditions, adenosine appears to induce predominant postglomerular vasodilatation, as well as preglomerular vasoconstriction when the renin-angiotensin system is activated. Theophylline, a xanthine with strong adenosine antagonistic properties, prevents the hypoxemia-induced renal changes, while enprofylline, a xanthine devoid of such properties, does not prevent these changes. Available data favor the hypothesis that intrarenal adenosine is involved in the pathophysiology of the renal changes observed in the early phase of vasomotor nephropathy.