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Lori L Woods

Publications and source records attributed to Lori L Woods.

7 recordsLinked to original sources
PubMed2006

Maternal glucocorticoids and prenatal programming of hypertension.

Maternal glucocorticoids have been postulated to play an important role in prenatal programming for adult hypertension in the offspring. However, we have shown previously that offspring hypertension caused by maternal dexamethasone subcutaneous administration at 100 microg x kg(-1) x day(-1) can be accounted for by the corresponding reduction in food intake that these mothers experience. The present studies were designed to determine whether there is a lower dose of dexamethasone that does not reduce maternal food intake yet still causes hypertension in the adult offspring. Pregnant rats were treated with subcutaneous dexamethasone at 50 (D50) or 25 (D25) microg x kg(-1) x day(-1) on days 15-20 of pregnancy. An additional group was untreated or received vehicle injections (control). D25 and D50 dams reduced their food intake by 17% during and after treatment and gained 31% less weight than control over the course of gestation. In adulthood ( approximately 21 wk), chronically instrumented male offspring of D50 and D25 had normal blood pressures (D50: 131 +/- 2 mmHg and D25: 127 +/- 3 mmHg vs. 127 +/- 2 mmHg in control). Qualitatively similar results were found in female offspring. Thus neither dexamethasone per se at these doses nor the accompanying modest reductions in maternal food intake and weight gain have blood pressure programming effects. As far as has been tested, there does not appear to be a dose of dexamethasone that, given over this time period in the rat, programs offspring hypertension without reducing maternal food intake and weight gain. These data do not support the hypothesis that maternal glucocorticoids program offspring hypertension directly.

Animals↗
PubMed2005

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

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 10(6) microm(3), LP vs. NP: 1.07 +/- 0.11 10(6) microm(3)); 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.

Animals↗
PubMed2005

Prenatal programming of adult blood pressure: role of maternal corticosteroids.

Both maternal glucocorticoid administration and maternal dietary protein or food restriction in pregnancy cause fewer nephrons and hypertension in the adult offspring. The purpose of these studies was to determine the extent to which nutritional factors contribute to programming of offspring hypertension by maternal glucocorticoids. Pregnant rats were treated with dexamethasone (100 microg x kg(-1) x d(-1) sc) on days 1-10 (ED) or days 15-20 (LD) of pregnancy. Additional groups of pregnant animals were pair fed to the early (EDPF) and late (LDPF) dexamethasone-treated groups, and another group was untreated or given vehicle (C). The dams treated with dexamethasone reduced their food intake and lost or failed to gain a normal amount of weight during treatment; body weights of ED dams caught up to normal after the treatment period, whereas those of LD dams did not. In adulthood ( approximately 21 wks), chronically instrumented male offspring of ED had normal blood pressures (125 +/- 2 mmHg vs. 126 +/- 1 mmHg in C), whereas LD offspring were hypertensive (136 +/- 3 mmHg). However, LDPF offspring were equally hypertensive (134 +/- 2 mmHg). Glomerular filtration rates normalized to body weight were not significantly different among groups. Qualitatively similar results were found in female offspring. Thus the long-term effects of maternal glucocorticoid administration at this dose on offspring's blood pressure may, in large part, be accounted for by the reduction in maternal food intake. These data suggest that maternal glucocorticoids and maternal food or protein restriction may, at least in part, share a common mechanism in programming offspring for hypertension. The window of sensitivity of future offspring blood pressure to either maternal insult coincides with nephrogenesis in the rat, suggesting that impaired renal development could play an important role in this programming.

Adrenal Cortex Hormones↗
PubMed2004

Naturally occurring intrauterine growth retardation and adult blood pressure in rats.

In humans, infants who are born small have been reported to have higher blood pressure in adulthood than do larger infants. This suggests that factors in the intrauterine environment that affect fetal growth can program the individual for hypertension later in life. The present study determined whether there is a similar, naturally occurring relationship between birth weight and adult blood pressure in rats. Female Sprague-Dawley rats bred in our colony were fed a normal diet during pregnancy. On the day of delivery, any pups that weighed <90% of the mean pup weight for the litter were identified as runts. For each runt, a sex-matched littermate of normal weight was also identified and assigned to this study. These pairs were chronically instrumented at approximately 20 wk of age. Mean arterial pressure was significantly higher in runt male and female offspring compared with their normal birth weight littermates (males: 149 +/- 7, runts versus 129 +/- 4 mmHg, controls; females: 128 +/- 1, runts versus 119 +/- 2 mmHg, controls). Although the runts had smaller body weights at study than did their littermate controls, the kidney-to-body weight ratio and renal function normalized to kidney or body weight were not different. These studies indicate that adult blood pressure is related to birth weight in rats, as it is in humans. The relative hypertension in runt animals is not due to gross differences in renal function but may be related to more subtle renal structural and/or functional differences.

Adrenal Glands↗
PubMed2004

Programming of adult blood pressure by maternal protein restriction: role of nephrogenesis.

BACKGROUND: Modest maternal protein restriction leads to hypertension and a reduced number of glomeruli in adult male but not female offspring. This study determined whether a more severe protein restriction has equivalent effects on male and female rat offspring, and examined the role of nephrogenesis in this programming. METHODS: Sprague-Dawley rats were fed a protein-restricted (5% protein) diet throughout (LLP), or during the first (LLP/NP) or second (NP/LLP) half of pregnancy. Controls ate a normal diet (NP, 19% protein). Adult offspring were chronically instrumented at 22 weeks; glomerular number and volume were estimated using stereologic techniques. RESULTS: Mean arterial pressures in male offspring were significantly higher in LLP (136 +/- 2 mm Hg) or NP/LLP (137 +/- 2 mm Hg) than in LLP/NP (125 +/- 1 mm Hg) or NP (125 +/- 2 mm Hg). Moreover, the hypertension was salt-sensitive (increase of 16 +/- 4 mm Hg in LLP on a high Na(+) diet compared to 2 +/- 2 mm Hg in NP). Glomerular number (per kidney) was reduced (15,400 +/- 2,411 in LLP vs. 27,208 +/- 1,534 in NP) but average individual glomerular volume was not different (1.98 +/- 0.18 106 micro(3) in LLP vs. 2.01 +/- 0.14 106 micro(3) in NP). Female offspring showed qualitatively similar results. CONCLUSION: Severe maternal dietary protein restriction reduces glomerular number and programs for salt-sensitive adult hypertension in both female and male offspring. The window of sensitivity of adult blood pressure to prenatal protein restriction falls within the period of nephrogenesis in the rat. These data are consistent with the hypothesis that maternal protein restriction causes adult hypertension in the offspring through impairment of renal development.

Aging↗
PubMed2002

Perinatal programming, renal development, and adult renal function.

Substantial data indicate that maternal diet during gestation, as well as perinatal events, affect organogenesis and, furthermore, may affect organ function at maturity, thus determining whether an individual is prone or resistant to a variety of health problems such as hypertension, cardiovascular disease, or renal dysfunction. This concept is called perinatal programming, or the fetal origins of adult disease (FOAD), a concept that arose after the publication of epidemiologic observations by Barker and colleagues that birth weight among apparently normal individuals studied in midlife was inversely associated with the presence of cardiovascular disease and hypertension. We now review evidence from studies in experimental animal models that have used nutritional and pharmacologic manipulation to extend epidemiologic observations.

Aging↗