Glomerular Hypertrophy in Offspring of Subtotally Nephrectomized Ewes

Brandon, Amanda E.; Boyce, A; Lumbers, Eugenie R.; Zimanyi, Monika A.; Bertram, John F.; Gibson, Karen J.

doi:10.1002/ar.20651

Cited by 12 publications

(24 citation statements)

References 26 publications

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“…It was concluded that these fetuses were exposed throughout pregnancy to an increased transplacental net flux of salt and water 7,8 and that this led to chronic suppression of renin secretion from the fetal kidneys. In contrast, by the second week after birth, the lambs were euvolaemic 4 . In particular, all the parameters that were used as indicators of increased transplacental fluid flux (baseline urine flow and sodium excretion rate, proximal tubular sodium handling, haematocrit, plasma chloride and plasma renin level) were similar to control lambs 4 …”

Section: Introductionmentioning

confidence: 85%

“…We have undertaken a number of studies into the effects of maternal renal dysfunction on renal development and function 2–6 . These experiments were in fetuses, newborn and 6‐month‐old lambs conceived and carried by ewes in which two‐thirds of their renal mass had been removed (by unilateral nephrectomy and partial infarction of the remaining kidney; STNx) at least 2 months before mating.…”

Section: Introductionmentioning

confidence: 99%

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Programming of the renin response to haemorrhage by mild maternal renal impairment in sheep

Brandon

Boyce

Lumbers

et al. 2011

Clin Exp Pharma Physio

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1. The aim of the present study was to test the hypothesis that the renin response to mechanisms activated by haemorrhage is programmed by exposure to maternal renal dysfunction. 2. In 26-27-day-old lambs born to ewes that had reduced renal function (STNxL, n=10) and lambs born to ewes with normal renal function (ConL, n=6), 1.6 mL/kg per min of blood was removed over 10 min. 3. Under basal conditions, the STNxL group had increased mean arterial pressure (P < 0.05). In response to haemorrhage, mean arterial pressure decreased in the STNxL group (P < 0.001), but there was no significant change in the ConL group. 4. Although plasma renin level increased in both groups (P < 0.05), the peak response was reduced and delayed in the STNxL group. In contrast, the rise in arginine vasopressin (AVP) level was similar in both groups and occurred over the same time course. At 24 h, both plasma renin and AVP level were the same as those measured before haemorrhage in both groups. Kidney renin level was similar in the two groups. 5. The attenuated renin response to haemorrhage in the STNxL group might explain the inability to maintain arterial pressure after haemorrhage. The results of the present study suggest that the renin response of the postnatal kidney to reductions in blood volume can be affected by the intrauterine environment. If these changes persist into adulthood, it suggests that permanent programming has occurred. Thus, the ability of an individual to respond to acute severe reductions in blood volume might be determined during intrauterine life.

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Section: Introductionmentioning

confidence: 85%

Section: Introductionmentioning

confidence: 99%

Programming of the renin response to haemorrhage by mild maternal renal impairment in sheep

Brandon

Boyce

Lumbers

et al. 2011

Clin Exp Pharma Physio

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“…Preparation of ANG- (1)(2)(3)(4)(5)(6)(7). ANG-(1-7) was obtained from Bachem BioScience (King of Prussia, PA).…”

Section: Animalsmentioning

confidence: 99%

“…SINCE ANTENATAL STEROID TREATMENT became the standard of care for enhancing fetal lung maturation in pregnancies threatened by premature labor between 24 and 34 wk of gestation, the use of corticosteroid therapy in the United States has increased from Ͻ15% of eligible pregnancies in 1990 to Ͼ75% in 1995 (1,3). However, clinical epidemiological studies show an association between antenatal glucocorticoid administration and altered vascular function (7,46), suggesting that exposure to excess glucocorticoids in the prenatal period may have untoward consequences in adult offspring.…”

mentioning

confidence: 99%

Gender differences in the effects of antenatal betamethasone exposure on renal function in adult sheep

Tang¹,

Carey²,

Bi³

et al. 2009

American Journal of Physiology-Regulatory, Integrative and Comp

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posure to clinically relevant doses of glucocorticoids during fetal life increases blood pressure in adult male and female sheep. The purpose of this study was to evaluate the effects of prenatal exposure to betamethasone at 80 -81 days of gestation on renal function in ewes and rams at 1.5 yr of age. In prenatal betamethasone-exposed males, compared with the vehicle-exposed animals, basal glomerular filtration rate (GFR) (1.93 Ϯ 0.08 vs. 2.27 Ϯ 0.10 ml ⅐ min Ϫ1 ⅐ kg body wt Ϫ1 ) and the ability to excrete an acute Na ϩ load (37.1 Ϯ 4.4 vs. 53.7 Ϯ 9.7%) were reduced. (P Ͻ 0.03 and P ϭ 0.03, respectively). In contrast, prenatal betamethasone exposure had no effect on basal GFR, Na ϩ excretion, or the percentage of the Na ϩ load excreted during the experiment in females. Systemic infusions of ANG-(1-7) at 9 ng⅐ min Ϫ1 ⅐ kg Ϫ1 for 2 h had minimal effects on basal GFR, renal plasma flow, and Na ϩ excretion in males but increased Na ϩ excretion in females. However, the percentage of Na ϩ load excreted during ANG-(1-7) infusion did not change in prenatal betamethasone-exposed females (113.1 Ϯ 14.2 vs. 98.1 Ϯ 12.2%) compared with the significant increase in vehicle females (139.2 Ϯ 22.3 vs. 92.2 Ϯ 7.5%) (P ϭ 0.01). The data indicate that antenatal betamethasone exposure produces gender-specific alternations in renal function and thus suggest that different mechanisms underlie the antenatal steroid-induced elevations in blood pressure in male and female offspring. prenatal steroid exposure; sodium load; glomerular filtration rate; sodium excretion; angiotensin-(1-7) SINCE ANTENATAL STEROID TREATMENT became the standard of care for enhancing fetal lung maturation in pregnancies threatened by premature labor between 24 and 34 wk of gestation, the use of corticosteroid therapy in the United States has increased from Ͻ15% of eligible pregnancies in 1990 to Ͼ75% in 1995 (1, 3). However, clinical epidemiological studies show an association between antenatal glucocorticoid administration and altered vascular function (7,46), suggesting that exposure to excess glucocorticoids in the prenatal period may have untoward consequences in adult offspring.We and others have shown using sheep and rat experimental models that prenatal steroid exposure results in elevated blood pressure in adulthood (8,10,14,36). Although there are likely multiple targets influencing the effect of steroids on blood pressure, several recent studies have suggested that altered kidney development induced by antenatal glucocorticoids may contribute to the elevations in arterial blood pressure (35,36,53). It is well known that the kidneys play a major role in the long-term regulation of arterial pressure and that change in renal function may lead to alterations in Na ϩ and water balance and blood pressure (19). In a rat model, Ortiz et al. (35,36) observed that prenatal exposure to dexamethasone on days 15 and 16 of gestation induced 30 and 20% reductions in glomerular number in offspring compared with controls when assessed at 60 -70 days and 6 -9 mo of age, ...

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“…2 Coupled with these findings are observations from animal studies that impaired maternal renal function during pregnancy leads to hyperfiltration by the fetus and neonate and to glomerulomegaly. 76 From early adult life, albuminuria is pervasive in Indigenous communities. 77 Therefore, as part of a cycle, there is evidence of renal damage in Aboriginal women of childbearing age.…”

Section: Role Of the Renal Ras In Adult Life In The Pathogenesis Of Cmentioning

confidence: 99%

The renin–angiotensin system from conception to old age: the good, the bad and the ugly

Lumbers

Pringle

Wang

et al. 2013

Clin Exp Pharma Physio

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The renin-angiotensin system (RAS) plays a critical role in placentation and nephrogenesis. Failure to thrive during intrauterine life, possibly related to placental dysfunction and impaired expression of the renal RAS, as well as prematurity, results in smaller kidneys at birth and reduced nephron number. The remaining nephrons are therefore hyperfiltering from birth. Hyperfiltration, infections and Type 2 diabetes cause glomerular and tubular fibrosis, leading to further reductions in nephron number. The intrarenal RAS plays a key role in promoting tubulointerstitial fibrosis. Low birth weight and a high incidence of preterm birth program Indigenous children for early onset renal disease in adult life. Indigenous Australians have 404 000 fewer nephrons than non-Indigenous Australians. This, coupled with the high incidence of infectious diseases (particularly acute post-streptococcal glomerulonephritis) and the increasing prevalence of Type 2 diabetes, explains why end-stage renal disease is of epidemic proportions in Indigenous Australians. The existence of RAS gene polymorphisms and inflammatory cytokines may further potentiate susceptibility to renal disease in Indigenous Australians.

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Glomerular Hypertrophy in Offspring of Subtotally Nephrectomized Ewes

Cited by 12 publications

References 26 publications

Programming of the renin response to haemorrhage by mild maternal renal impairment in sheep

Programming of the renin response to haemorrhage by mild maternal renal impairment in sheep

Gender differences in the effects of antenatal betamethasone exposure on renal function in adult sheep

The renin–angiotensin system from conception to old age: the good, the bad and the ugly

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