Renin cells are normally located in juxtaglomerular (JG) position in the afferent arterioles at the glomerular entrance. Under renin expression stimulating maneuvers like low salt (LS) diet and ACE inhibition, cells from the upper vessel wall are recruited in a retrograde manner to finally enhance renin production. The factors influencing this recruitment of renin producing cells are still unknown. Previous experiments indicate that the differentiation factor TGFb could be involved in renin expression regulation. It was found that renin cells express the TGFb receptor 2 and that its expression is co regulated with renin expression starting already during nephrogenesis in which renin cell recruitment occurs as well. The aim of our study is to investigate if the local absence of TGFbRII in renin producing cells does influence the renin cell recruitment in adult mouse kidneys. For this purpose we used local TGFbRII renCreflfl knockout mice, in which the TGFbRII is knocked out only in renCre reading cells. With the aid of 3D renal arterial tree reconstructions of LS and Enalapril treated knockout mice and their corresponding controls the renin distribution pattern was researched. To confirm the results on molecular level, western blot analysis and real time PCR measurements of TGFbRII and renin expression were performed. It could be observed that the distribution pattern of renin and its level of mRNA expression do not significantly differ in the knockout mouse under standard conditions as well as under LS diet and ACE inhibition. The knockout shows just a tendency to a slightly elevated renin level and is still able to up regulate renin expression. Therefore we think that the TGFbRII in renin expressing cells is not necessary for renin cell recruitment in the adult mouse kidney. Next step of our research will be to elucidate whether TGFb is important for renin cell shift during mural nephrogenesis.