The salt balance of the organism controls the number of renin producing cells in the kidney in an inverse fashion by yet undefined mechanisms. This study aimed to assess a possible mediator role of preglomerular blood pressure in the control of renin expression by oral salt intake. For our investigations we used mice lacking angiotensin II (ANGII) type 1a (AT_1a) receptors, because these mice display an enhanced salt sensitivity of renin expression. Utilizing 3-dimensional tissue reconstructions of the kidneys we found renin expressing cells along the preglomerular vascular tree in a typical corticomedullary distribution gradient, which was most prominent at high salt intake and which was nivellated by low salt intake. The breakdown of the distribution gradient from afferent arterioles to arcuate arteries went in parallel with sinks of the systolic blood pressure induced by reductions of sodium intake. Setting unilateral renal artery stenosis in mice on normal salt intake produced a similar distribution pattern of renin expressing cells, as did low salt intake. Conversely, increasing blood pressure by administration of the NOS-inhibitor L-NAME in mice kept on low salt intake produced a similar distribution pattern of renin producing cells as did high salt intake alone. These findings suggest that the influence of salt intake on the number and distribution of renin producing cells in ANGII-AT_1a deficient mice cannot be distinguished from changes of the preglomerular blood pressure.