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Should not yet change practice in congenital kidney disease; extends developmental biology insights but remains hypothesis-generating.
The renin-angiotensin system (RAS) plays a key role in cardiovascular homeostasis through the interactions of angiotensin II with its receptors. All components of the RAS are developmentally regulated in the kidney. The functions of the system in the maturing kidney overlap those of the adult, but higher levels of expression and novel locations of expression in the fetus suggest that the RAS has alternate functions as well. Increasing evidence suggests that the RAS may regulate renal growth and development by initiating a complex cascade of events, involving growth factors and proto-oncogenes and other unidentified factors. These same cascades may also be important in renal disease states. Recent advances in the field of molecular and cell biology are providing new tools and strategies to elucidate the intimate mechanism whereby the RAS regulates growth processes and disease states.
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Harris et al. (1997) studied this question.
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