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Abstract
Postnephrectomy serum has been proved to enhance proliferation of mesangial cells in culture. Studies in offspring to uninephrectomized (UNx) mothers indicate that it remains active for a long period following UNx. On the other hand, postnephrectomy renal compensatory growth in vivo is known to be completed within a short period. In this study we assessed the proliferative responses of mesangial cells from single kidneys of rats which were cultured 48 h or 4 months following contralateral nephrectomy. The proliferative stimulus was provided by different postnephrectomy sera. Proliferation of both experimental cell populations was significantly greater than that of controls. Moreover, the proliferation rate of early postcontralateral nephrectomy mesangial cells was greater than those harvested 4 months after nephrectomy. We, therefore, propose that the early in vivo completion of single kidney compensatory hypertrophy, at least in part, is due to progressive blunting of renal cell responsiveness to the mitotic stimulus of the animal's serum.
Key Words
Mesangial cells
Compensatory renal hypertrophy
Introduction
Compensatory renal growth following contralateral nephrectomy is a relatively rapid process, most of which being completed during a short period. In rats for example, the process has been shown to take about 10-28 days [1].
The nature of the stimuli responsible for this phenomenon has not been fully elucidated and, in fact, is still controversial. In a previous investigation we have shown that mice and rat pups born to mothers uninephrectomized prior to conception had exaggerated renal mass, protein content and number of glomeruli per kidney [2]. This was true whether conception took place early or late following removal of the kidney. These results strongly suggest the activation, following uninephrectomy (UNx), of a maternal humoral agent(s), which stimulates renal compensatory growth and which is sustained in her blood long after UNx. Indeed, postuninephrectomy serum has been shown to stimulate mesangial cell proliferation in vitro [3].
These data are difficult to reconcile with the known observation that renal compensatory hypertrophy in vivo is completed within a short period following UNx [4]. This could be due to alterations in the activity of the humoral factor(s) or, alternatively, to the development with time of a blunted responsiveness of renal cells to the proliferative stimulus of this factor(s).
The present study was undertaken to...