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1 Division of Nephrology and Hypertension, Oregon Health & Science University, Portland, OR, USA
2 Pediatric Nephrology Unit, Massachusetts General Hospital, Boston, MA, USA
3 Department of Cell Biology, Institute of Anatomy, University of Aarhus, Aarhus, Denmark
* To whom correspondence should be addressed. E-mail: woodsl{at}ohsu.edu.
Modest maternal dietary protein restriction in the rat leads to hypertension in adult male offspring. The purpose of this study was to determine whether female rats are resistant to developing the increased blood pressure seen in males following maternal protein restriction. Pregnant rats were fed a normal (19%, NP) or low (8.5%, LP) protein diet throughout gestation. Renal renin protein and ANGII levels were reduced by 50-65% in male LP compared to NP pups, but were not suppressed in female LP compared to female NP. Mean arterial pressure in conscious, chronically instrumented adult female offspring (21 wks) was not different in LP (120±3 mmHg, LP vs. 121±2 mmHg, NP), and glomerular filtration rate was also not different in LP vs. NP. The number of glomeruli per kidney was similar in adult LP and NP female offspring (26,050±2,071, LP vs. 26,248±1,292, NP), and individual glomerular volume was also not different (0.92±0.11 106 µ3, LP vs. 1.07±0.11 106 µ3, NP); the total volume of all glomeruli per kidney was also not significantly different. Thus, female rats are relatively resistant to the programming for adult hypertension by perinatal protein restriction that we have described in males. This resistance may be due to the fact that modest maternal protein restriction does not reduce the number of glomeruli with which females are endowed as it does in males. The intrarenal RAS during development may play a key role in this protective effect of female gender.
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