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1 Anatomy & Cell Biology, Monash University, Melbourne, Victoria, Australia
2 Physiology, Monash University, Melbourne, Victoria, Australia
3 Anatomical Pathology, Alfred Hospital, Melbourne, Victoria, Australia
* To whom correspondence should be addressed. E-mail: chantal.hoppe{at}med.monash.edu.au.
ABSTRACT The effects of prenatal protein restriction on adult renal and cardiovascular function have been studied in considerable detail. However, little is known regarding the effects of life-long protein restriction, a common condition in the developing world. Therefore, we determined in rats the effects of combined pre- and post-natal protein restriction on adult arterial pressure and renal function, and responses to increased dietary sodium. Nephron number was also determined. Male Sprague-Dawley rats were born to mothers fed a low (8 % w/w; LP) or normal (20 % w/w; NP) isocaloric protein diet throughout pregnancy, and maintained on these diets after birth. At postnatal day 135, nephron number, mean arterial pressure (MAP) and renal function were determined. A high NaCl (8.0 % w/w) diet (high salt) was fed to a subset of rats from weaning. MAP was less in LP- than NP-rats (120±2 versus 128±2 mmHg; P<0.05) and was not significantly altered by increased salt intake. Nephron number was 31% less in LP- than NP-rats (P<0.001). The volume of individual glomeruli was also less in LP- than NP-rats, as were calculated effective renal plasma flow (ERPF) and glomerular filtration rate (GFR). GFR but not ERPF appeared to be increased by high salt intake, particularly in LP rats. In conclusion, protein restriction induced a severe nephron deficit, but MAP was lower, rather than higher than control rats in adulthood. These findings indicate that the post-natal environment plays a key role in determining the outcomes of developmental programming.
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