Introduction that sympathetic nerve stimulation or addition of nor-For many years catecholamines are known to particip-adrenaline decreases the diameter of the glomeruli [5]. ate in the regulation of glomerular blood flow and A decrease in K f after sympathetic nerve stimulation microcirculation, mainly by influencing cellular func-may at least partially be due to a reduction of glomertions of the renal vascular and the glomerular mesang-ular surface area. In mesangial cells, noradrenaline ium [1]. Until recently knowledge about the actions of increases the uptake of Ca2+ and induces a cell contraccatecholamines on cells from the glomerular filtration tion [6, 7]. Thus, it has been suggested that noradrenabarrier is, due to their unique localization, limited. line-induced mesangial cell contraction might decrease These cells, ie podocytes and glomerular endothelial K f by a reduction of the capillary surface area [7]. cells are probably involved in the control of glomerular However, noradrenaline might not only contract meshaemodynamics and filtration. Especially the podocyte angial cells but also podocyte foot processes, which seems to be an important regulator of glomerular are known to possess a rich contractile apparatus [8]. functions: it stabilizes the glomerular architecture, Noradrenaline-induced contraction of foot processes maintains a large filtration surface, and serves as an might also lead to a reduced capillary surface area and effective barrier to plasma proteins [2]. Very recently decreased K f

. It appears difficult to prove this Mundel et al. successfully propagated differentiated hypothesis, but a detection of noradrenaline-induced podocytes in cell culture, thus allowing the study of changes of podocyte function may support its validity. biological properties of these cells in vitro [3]. This