As discussed above, in a similar model of maternal undernutrition, plasma levels of the anorexigenic leptin were increased and levels of the orexigenic prolactin were decreased. In addition to decreasing maternal food intake, this hormone imbalance could have imprinted an impaired dietary behavior on the progeny. Evidence for this concerns elevated plasma levels of leptin in 
pups from mothers that had been undernourished during lactation, as a result of direct transmission via milk. Acid maceration is not the gold-standard method for estimating the Pimozide number of nephrons. However, reproducibility of counting using Lomitapide Mesylate different kidneys and more than one independent observer, together with comparable control values with data from other laboratories, demonstrated a profound influence of programming in terms of the number of nephrons in adult kidneys. The reduced number of nephrons and the structural glomerular alterations demonstrate that the decreased kidney mass of programmed animals was not a simple relationship to lower body mass. The decreased number of nephrons and decreased capillary area with consequent hypofiltration could be associated with hyperfiltration in remnant healthy nephrons, where the increased intracapillary pressure would contribute to their late and progressive self-destruction with late onset hypertension. The onset of hypertension in older rats supports this view. An increase in the glomerular area would be expected when the number of nephrons is decreased, and compensatory hyperfiltration occurs in some remnant glomeruli. It could be that intense collagen deposition in the cortex of programmed animals affects many glomerular structures, causing a global reduction in the size of the Bowman’s capsule and glomerular capillary tufts, with preservation or an increase in the area of others. It is unexpected that GFR increases by 70% in 60 day-old programmed rats, despite reduced glomerular areas as presented in Fig. 4. However, this could be explained by exacerbated hyperfiltration in the preserved nephrons. The intense proteinuria that accompanies the increase in GRF and UNa reveals important and early damage in the filtration barrier that could evolve into global impairment of renal function in programmed rats. Therefore, kidneys from progeny that were programmed during lactation suffer from early severe morphological, and consequently functional, alterations in glomerular components, adding to the molecular alterations in proximal tubules, as discussed below. The results depicted in Figs. 6, 7, 8, 9 demonstrate that programming during lactation strongly imprints the molecular machinery responsible for the majority of Na + absorption and the fine tuning of this process, leading to augmented recovery of the filtered fluid, which can subsequently contribute to the onset of hypertension. It is interesting that placental undernutrition promotes different modifications from those observed in the present study of young adult rats. This supports the view that depending on the window of development, undernutrition may evoke different signals that affect the same organs in different ways. Up-regulation of AT1 receptors and down-regulation of AT2 receptors could represent the persistence into adulthood of an adaptative response towards impaired RAS functioning in early life. Lower local Ang II production in early life could be compensated by the programming-induced reciprocal alterations in the populations of AT1 and AT2 receptors as demonstrated in Fig. 10, which persisted into adult life. In contrast to the results concerning active Na + transporters.