Modest maternal protein restriction fails to program adult hypertension in female rats

2005 ◽  
Vol 289 (4) ◽  
pp. R1131-R1136 ◽  
Author(s):  
Lori L. Woods ◽  
Julie R. Ingelfinger ◽  
Ruth Rasch
Keyword(s):  
Renin Angiotensin System ◽  
Female Gender ◽  
Female Offspring ◽  
Protein Restriction ◽  
Female Rats ◽  
Male Rats ◽  
Pregnant Rats ◽  
Angiotensin System ◽  
Low Protein ◽  
Maternal Protein Restriction

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 106μm3, LP vs. NP: 1.07 ± 0.11 106μm3); 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.

scholarly journals Maternal protein restriction differentially alters the expression of AQP1, AQP9 and VEGFr-2 in the epididymis of rat offspring

2019 ◽  
Vol 20 (3) ◽  
pp. 469 ◽  
Author(s):  
Marilia Martins Cavariani ◽  
Talita de Mello Santos ◽  
Dhrielly Natalia Pereira ◽  
Luiz Gustavo de Almeida Chuffa ◽  
Patricia Fernanda Felipe Pinheiro ◽  
...  
Keyword(s):  
Protein Restriction ◽  
Male Rats ◽  
Standard Diet ◽  
Vascular Endothelial ◽  
Pregnant Rats ◽  
Low Protein ◽  
Maternal Protein Restriction ◽  
Endothelial Growth Factor ◽  
Development Methods ◽  
Protein Diets

Background: Maternal protein restriction causes sperm alterations in the offspring, most of which are associated with epididymal functions. Because fluid reabsorption/secretion dynamics in the epididymal environment play important roles in the process of sperm maturation and concentration, we investigated the effects of maternal protein restriction on the expression of aquaporins (AQP1 and AQP9), vascular endothelial growth factor (VEGFa), and its receptor VEGFr-2 in different stages of postnatal epididymal development. Methods: Pregnant rats were divided into groups that received normoprotein (17% protein) and low-protein diets (6% protein) during gestation and lactation. After weaning, male rats only received the standard diet and were euthanized at the predetermined ages of 21, 44 and 120 days. Results: Maternal protein restriction decreased AQP1 and AQP9 expression in the initial segment and caput epididymis compared to the increased expression of these proteins observed in the corpus and cauda at all ages. Although protein restriction reduced the microvasculature density (MVD) on postnatal day (PND) 21 and 44, the MVD was unaltered on PND 120. Conclusions: Maternal protein restriction changed the structure or function of the offspring’s epididymis, specifically by affecting fluid dynamics and vasculogenesis in important stages of epididymis development.

scholarly journals Maternal Protein Restriction Modulates Angiogenesis and AQP9 Expression Leading to a Delay in Postnatal Epididymal Development in Rat

Cells ◽  
2019 ◽  
Vol 8 (9) ◽  
pp. 1094 ◽  
Author(s):  
Talita de Mello Santos ◽  
Marilia Martins Cavariani ◽  
Dhrielly Natália Pereira ◽  
Bruno César Schimming ◽  
Luiz Gustavo de Almeida Chuffa ◽  
...  
Keyword(s):  
Well Being ◽  
Protein Restriction ◽  
Protein Diet ◽  
Low Protein Diet ◽  
Pregnant Rats ◽  
Low Protein ◽  
Maternal Protein Restriction ◽  
Aqp1 Expression ◽  
In The Beginning ◽  
Endothelial Growth Factor

The maternal nutritional status is essential to the health and well-being of the fetus. Maternal protein restriction during the perinatal stage causes sperm alterations in the offspring that are associated with epididymal dysfunctions. Vascular endothelial growth factor (VEGF) and its receptor, VEGFr-2, as well as aquaporins (AQPs) are important regulators of angiogenesis and the epididymal microenvironment and are associated with male fertility. We investigated the effects of maternal protein restriction on epididymal angiogenesis and AQP expression in the early stages of postnatal epididymal development. Pregnant rats were divided into two experimental groups that received either a normoprotein (17% protein) or low-protein diet (6% protein) during gestation and lactation. At postnatal day (PND)7 and PND14, male offspring were euthanized, the epididymides were subjected to morphometric and microvascular density analyses and to VEGF-A, VEGF-r2, AQP1 and AQP9 expression analyses. The maternal low-protein diet decreased AQP9 and VEGFr-2 expression, decreased epididymal microvascularity and altered the morphometric features of the epididymal epithelium; no changes in AQP1 expression were observed at the beginning of postnatal epididymal development. Maternal protein restriction alters microvascularization and affects molecules involved in the epidydimal microenvironment, resulting in morphometric alterations related to a delay in the beginning of epididymis postnatal development.

Maternal protein restriction compromises myocardial contractility in the young adult rat by changing proteins involved in calcium handling

2016 ◽  
Vol 120 (3) ◽  
pp. 344-350 ◽  
Author(s):  
Aucelia C. S. de Belchior ◽  
David D. Freire ◽  
Carlos P. da Costa ◽  
Dalton V. Vassallo ◽  
Alessandra S. Padilha ◽  
...  
Keyword(s):  
Cardiovascular Risk ◽  
Young Adult ◽  
Left Ventricular ◽  
Protein Restriction ◽  
Female Rats ◽  
Male Rats ◽  
Calcium Handling ◽  
Myocardial Mechanics ◽  
Maternal Protein Restriction ◽  
Calcium Handling Proteins

Maternal protein restriction (MPR) during pregnancy is associated with increased cardiovascular risk in the offspring in adulthood. In this study we evaluated the cardiac function of young male rats born from mothers subjected to MPR during pregnancy, focusing on the myocardial mechanics and calcium-handling proteins. After weaning, rats received normal diet until 3 mo old, when the following parameters were assessed: arterial and left ventricular hemodynamics and in vitro cardiac contractility in isolated papillary muscles. The body weight was lower and arterial pressure higher in the MPR group compared with young adult offspring of female rats that received standard diet (controls); and left ventricle time derivatives increased in the MPR group. The force developed by the cardiac muscle was similar; but time to peak and relaxation time were longer, and the derivatives of force were depressed in the MPR. In addition, MPR group exhibited decreased post-pause potentiation of force, suggesting reduced reuptake function of the sarcoplasmic reticulum. Corroborating, the myocardial content of SERCA-2a and phosphorylated PLB-Ser16/total PLB ratio was decreased and sodium-calcium exchanger was increased in the MPR group. The contraction dependent on transsarcolemmal influx of calcium was higher in MPR if compared with the control group. In summary, young rats born from mothers subjected to protein restriction during pregnancy exhibit changes in the myocardial mechanics with altered expression of calcium-handling proteins, reinforcing the hypothesis that maternal malnutrition is related to increased cardiovascular risk in the offspring, not only for hypertension, but also cardiac dysfunction.

scholarly journals Diabetes in Old Male Offspring of Rat Dams Fed a Reduced Protein Diet

2001 ◽  
Vol 2 (2) ◽  
pp. 139-143 ◽  
Author(s):  
Clive J. Petry ◽  
Matthew W. Dorling ◽  
Dorota B. Pawlak ◽  
Susan E. Ozanne ◽  
C. Nicholas Hales
Keyword(s):  
Insulin Resistance ◽  
Glucose Tolerance ◽  
Protein Restriction ◽  
Male Rats ◽  
Male Rat ◽  
Intravenous Glucose ◽  
Low Protein ◽  
Maternal Protein Restriction ◽  
Increased Risk ◽  
Intravenous Glucose Tolerance Tests

Restricted fetal growth is associated with increased risk for the future development of Type 2 diabetes in humans. The study aim was to assess the glucose tolerance of old (seventeen months) male rats, which were growth restricted in early life due to maternal protein restriction during gestation and lactation. Rat mothers were fed diets containing either 20% or 8% protein and all offspring weaned onto a standard rat diet. In old-age fasting plasma glucose concentrations were significantly higher in the low protein offspring: 8.4 (1.3)mmol/l v. 5.3 (1.3)mmol/l (p = 0.005), Areas under the curves were increased by 67% for glucose (p = 0.01) and 81% for insulin (p = 0.01) in these rats in intravenous glucose tolerance tests, suggesting (a degree of) insulin resistance. These results show that early growth retardation due to maternal protein restriction leads to the development of diabetes in old male rat offspring. The diabetes is predominantly associated with insulin resistance.

Malaoxon-Induced Brain Phosphoinositide Turnover and Changes in Brain Calcium Levels by Female Gender in Pregnant and Non-Pregnant Convulsing and Non-Convulsing Rats

1993 ◽  
Vol 12 (6) ◽  
pp. 469-477 ◽  
Author(s):  
M.-R. Hirvonen ◽  
K.M. Savolainen
Keyword(s):  
Young Male ◽  
Female Gender ◽  
Pregnant Female ◽  
Female Rats ◽  
Male Rats ◽  
Adult Rats ◽  
Pregnant Rats ◽  
Inositol 1 ◽  
Pi Turnover ◽  
Clonic Convulsions

Alterations in malaoxon-(MO)-induced brain regional phosphoinositide (PI) turnover and in brain calcium levels were studied in female non-pregnant and pregnant rats, and in their offspring. The adult rats were followed for 1 or 4 h after MO for tonic-clonic convulsions. A dose of 8.2 mg kg-1 of MO caused similar convulsions in 74% of the pregnant rats as we have reported in young male rats with a dose of 39.2 mg kg-1,1 However, convulsions did not occur in non-pregnant female rats. Inositol and inositol monophosphate levels were similar in all control rats. MO decreased brain inositol both in pregnant and non-pregnant female rats, and in the cerebellum of the offspring. In contrast to the findings in male rats, MO only randomly increased brain inositol-1-phosphate in female rats, or in their offspring. However, cerebral inositol-4-phosphate levels were similarly increased both in the non-pregnant and the pregnant rats irrespectively of convulsions. MO did not elevate cerebral Ca2+ in female rats or their offspring, in contrast to the male rats. 1 The present results suggest that female rats are more sensitive than male rats to MO-induced PI signalling, and during pregnancy, also to MO-induced overt convulsions, but not to changes in cerebral Ca2+.

scholarly journals Sex-related differences in the intratubular renin-angiotensin system in two-kidney, one-clip hypertensive rats

2019 ◽  
Vol 317 (3) ◽  
pp. F670-F682 ◽  
Author(s):  
Sang Ho Lee ◽  
Yu Ho Lee ◽  
Su Woong Jung ◽  
Dong Jin Kim ◽  
Seon Hwa Park ◽  
...  
Keyword(s):  
Renal Artery ◽  
Renin Angiotensin System ◽  
Female Rats ◽  
Male Rats ◽  
Ang Ii ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Mas Receptor

The intratubular renin-angiotensin system (RAS) is thought to play an essential role in hypertensive renal disease, but information regarding sex-related differences in this system is limited. The present study investigated sex differences in the intratubular RAS in two-kidney, one-clip (2K1C) rats. A 2.5-mm clip was placed on the left renal artery of Sprague-Dawley rats, and rats were euthanized 3 or 5 wk after the operation. Systolic blood pressure increased in 2K1C rats in both sexes but was significantly higher in male rats than in female rats, and an antihypertensive effect was not observed in 2K1C ovariectomized (OVX) female rats. Compared with male 2K1C rats, intratubular angiotensin-converting enzyme (ACE) and ANG II were repressed, and intratubular ACE2, angiotensin (1–7), and Mas receptor were increased in both kidneys in female 2K1C rats 5 wk after surgery. Comparison with male and female rats and intratubular mRNA levels of ACE and ANG II type 1 receptor were augmented in OVX female rats, regardless of the clipping surgery 3 wk postoperation. ANG II type 2 receptor was upregulated in female rats with or without OVX; thus, the ANG II type 1-to-type 2 receptor ratio was higher in male rats than in female rats. In conclusion, female rats were protected from hypertensive renal and cardiac injury after renal artery clipping. An increase in the intratubular nonclassic RAS [ACE2/angiotensin (1–7)/Mas receptor] and a decrease in the ANG II type 1-to-type 2 receptor ratio could limit the adverse effects of the classic RAS during renovascular hypertension in female rats, and estrogen is suggested to play a primary role in the regulation of intratubular RAS components.

Brain Renin-Angiotensin System: Fetal Epigenetic Programming by Maternal Protein Restriction During Pregnancy

2009 ◽  
Vol 17 (3) ◽  
pp. 227-238 ◽  
Author(s):  
Ravi Goyal ◽  
Dipali Goyal ◽  
Arthur Leitzke ◽  
Ciprian P. Gheorghe ◽  
Lawrence D. Longo
Keyword(s):  
Renin Angiotensin System ◽  
Protein Restriction ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Maternal Protein Restriction ◽  
Epigenetic Programming
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