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DEVELOPMENTAL PHYSIOLOGY AND PREGNANCY
1Division of Nephrology and Hypertension, Oregon Health & Science University, Portland, Oregon; 2Pediatric Nephrology Unit, Massachusetts General Hospital, Boston, Massachusetts; and 3Department of Cell Biology, Institute of Anatomy, University of Aarhus, Aarhus, Denmark
Submitted 23 January 2003 ; accepted in final form 10 June 2005
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 male rats after maternal protein restriction. Pregnant rats were fed a normal protein (19%, NP) or low-protein (8.5%, LP) diet throughout gestation. Renal renin protein and ANG II levels were reduced by 50–65% in male LP compared with NP pups, but were not suppressed in female LP compared with female NP. Mean arterial pressure in conscious, chronically instrumented adult female offspring (22 wk) was not different in LP (LP: 120 ± 3 mmHg vs. NP: 121 ± 2 mmHg), 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 (LP: 26,050 ± 2,071 vs. NP: 26,248 ± 1,292, NP), and individual glomerular volume was also not different (LP: 0.92 ± 0.11 106 µm3, LP vs. NP: 1.07 ± 0.11 106 µm3); 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 renin-angiotensin system during development may play a key role in this protective effect of female gender.
perinatal programming; nephron number; gene expression; gender; renin-angiotensin system
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