In maximally vasodilated SHR and NCR kidneys, perfused with filtrable and non-filtrable perfusates, analyses have been performed concerning the extent of average renal tissue pressure (Pt) elevation which occurs upon glomerular filtration and causes passive autoregulation of flow. The results illustrate the great importance of distinguishing between 'apparent' (PA--PV/flow) and 'true' (PA--Pt/flow) renal resistance to flow. This is particularly so when the compared SHR and NCR renal vascular beds differ not only in true total renal resistance but also concerning the structurally determined ratio between the pre- and post-glomerular resistances. The combined results show that this ratio is considerably elevated in adults SHT kidneys because of structural vascular changes, which is perhaps the most efficient way of resetting the 'long term barostat function' of the kidneys in hypertension. It is also illustrated how the altered pre-/post-glomerular ratio in SHR in combination with Pt rises can so markedly distort the results of apparently precise in vitro comparisons of SHR and NCR renal vascular beds as to give entirely misleading results, with underestimations of the structurally based vascular hyperreactivity of the preglomerular section in SHR.