Relation of distal tubular NaCl delivery and glomerular hydrostatic pressure. We have tested certain aspects of the hypothesis that the rate of distal tubular sodium delivery determines the rate of filtration in that nephron. Schnermann, Wright et al have suggested that a reduction in distal sodium delivery causes the local release of angiotensin which acts to elevate the glomerular hydrostatic pressure (P_G) of that nephron by constricting the efferent arteriole, thereby increasing the nephron filtration rate. We have, therefore, examined the influence of distal sodium delivery upon glomerular hydrostatic pressure utilizing a servo null pressure device in Wistar rats with surface glomeruli on normal NaCl diet (Group I), low NaCl diet (Group II) and during saline diuresis (Group III). Glomerular pressure was quite similar in all three groups. In single nephron studies, in these same three groups, an acute reduction in distal sodium delivery did not alter nephron glomerular hydrostatic pressure. We conclude: 1) mechanisms exist whereby P_G is autoregulated despite acute tubular obstruction and wide variations in distal sodium delivery; 2) if nephron filtration rate rises with reduction in distal sodium delivery, this must be mediated by increased plasma flow to that nephron, since glomerular hydrostatic pressure is unchanged.