The occurrence of vacuoles in cells of contractile tissues and especially in media cells of resistance vessels has been known for quite some time. Recently, it has been widely accepted that these vacuoles, characteristically lined by a double membrane, result from herniation of one vascular smooth muscle cell into the other as a result of vasoconstriction. In our electronmicroscopic investigations we found double membrane-bounded vacuoles not only in kidney resistance vessels of rats and mice under conditions of vasoconstriction, but also in control animals and animals with maximal renal vasodilation. Part of our observations are compatible with the assumption that such vacuoles arise from a damage of club-shaped, musculo-muscular contacts due to shape changes of media cells during maximal vasoconstriction or vasodilation. However, serial thin sectioning revealed that some of the cytoplasmic vacuoles have no connections with neighbouring cells. This finding and various parallels to the generation of autophagic vacuoles indicate that the so-called herniations may also represent demarcations of large cytoplasmic areas within an individual cell. Irrespective of the origin of these vacuoles, their contents show different stages of deterioration. At later stages, the vacuoles appear to be adjacent, with only one membrane, to the extracellular space, into which they are believed to discharge finally. Cytoplasmic vacuolization has not only been observed in smooth muscle cells, but also in juxtaglomerular epithelioid cells of the afferent arteriole. Here the vacuoles-besides other organelles--also contain secretory granules; it is therefore proposed that autophagic phenomena with final extrusion of cytoplasmic material may be involved in the programmed down-regulation of the granular renin store following inhibition of renin synthesis and secretion.