Review: Sex specific programming: A critical role for the renal renin–angiotensin system

Moritz, Karen M.; Cuffe, James; Wilson, Leticia; Dickinson, Hayley; Wlodek, Mary E.; Simmons, David G.; Denton, Kate M.

doi:10.1016/j.placenta.2010.01.006

Cited by 108 publications

(103 citation statements)

References 55 publications

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“…57 Importantly, alterations to the RAS have been evidenced in a number of animal models of hypertension programming. 58 In preterm neonates, the urinary angiotensin-converting enzyme activity is increased compared with infants born at term, with a significant inverse association between angiotensin-converting enzyme activity and both gestational and postnatal age. 59 However, very few studies have been conducted in this area, and further research is undoubtedly required to understand the potential role of the RAS in the programming of high blood pressure after preterm birth.…”

Section: Renin-angiotensin Systemmentioning

confidence: 99%

Preterm Birth and Hypertension Risk

et al. 2014

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Section: Renin-angiotensin Systemmentioning

confidence: 99%

Preterm Birth and Hypertension Risk

et al. 2014

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“…The renin-angiotensin system (RAS) is also implicated in some of these programing outcomes. Specifically, the RAS is often suppressed during renal development, potentially contributing to the nephron deficit, followed by a compensatory increase in activity in postnatal life (Moritz et al 2010). Given the integral role of the RAS in fluid balance and blood pressure control in the adult, long-term upregulation of this system, combined with the low nephron endowment, provides a highly plausible pathway through which prenatal insults may result in hypertension.…”

Section: Effects On Nephron Numbermentioning

confidence: 99%

Adverse prenatal environment and kidney development: implications for programing of adult disease

Dorey¹,

Pantaleon²,

Weir³

2014

Reproduction

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The 'developmental origins of health and disease' hypothesis suggests that many adult-onset diseases can be attributed to altered growth and development during early life. Perturbations during gestation can be detrimental and lead to an increased risk of developing renal, cardiovascular, metabolic, and neurocognitive dysfunction in adulthood. The kidney has emerged as being especially vulnerable to insult at almost any stage of development resulting in a reduction in nephron endowment. In both humans and animal models, a reduction in nephron endowment is strongly associated with an increased risk of hypertension. The focus of this review is twofold: i) to determine the importance of specific periods during development on long-term programing and ii) to examine the effects of maternal perturbations on the developing kidney and how this may program adult-onset disease. Recent evidence has suggested that insults occurring around the time of conception also have the capacity to influence long-term health. Although epigenetic mechanisms are implicated in mediating these outcomes, it is unclear as to how these may impact on kidney development. This presents exciting new challenges and areas for research.Reproduction (2014) 147 R189-R198

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“…18 Animal studies have recapitulated these findings and allowed exploration of the underlying mechanisms, which are sexually dimorphic. 12,19 Testosterone has been clearly demonstrated to contribute to the programming of adult hypertension in growth-restricted male rat offspring. 20 Recently, this same group has defined a role for increased oxidative stress in determining kidney function and arterial pressure in growth-restricted male offspring, an effect that was reversed by antioxidant therapy.…”

Section: Sex-related Differences In the Trajectory Of Arterial Pressumentioning

confidence: 99%

Sex-Related Differences in Hypertension

2013

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M uch of what we understand about the regulation of arterial pressure and extracellular fluid volume has been derived from studies in men. Although the responses that can be mounted against major physiological challenges to extracellular fluid volume (hemorrhage/dehydration) are essentially similar in men and women, there are marked sex-related differences in the regulation of renal and cardiovascular physiology. These possibly underpin the greater risk of renal and cardiovascular disease (CVD) in men and, conversely, confer the relative protection from these conditions in women, at least until menopause. In recent years, advances have been made in understanding the mechanistic bases for sex-related differences in CVD and these have been reviewed in detail.1-3 Therefore, the purpose of this report is to provide an update of findings in the past few years. Sex-Specific Risk Factors and Clinical OutcomesIncreasingly, studies are incorporating sex as a factor into their analyses.Although not all studies demonstrate a sex-specific interaction, 4-7 many do, exemplifying the mantra, seek and ye shall find; this appears to be particularly true for sex-related differences in CVD. In recent years, evidence that women have smaller and stiffer hearts because of a greater collagen content has received a good deal of attention for the reason that it may explain some of the puzzling differences in clinical signs of CVD between men and women. Puntmann et al 8 examined aortic stiffness by pulse wave velocity and ventricular deformation indices using MRI both at rest and during dobutamine challenge in elderly men and women. At rest, women had greater aortic stiffness and ventricular deformation than men. Moreover, sex-related differences were observed during stress because men had increased longitudinal and circumferential ventricular deformation during dobutamine challenge, whereas women only had an increase in circumferential deformation. 8 These data suggest that differential loading of the aortic reservoir in men occurs because of increases in longitudinal and circumferential ventricular contraction, an effect independent of aortic stiffness. However, dynamic challenge with dobutamine induced only a limited response in women, because although men could improve longitudinal ventricular contraction, women could not. Russo et al 9 reported similar findings of increased arterial stiffness and wave reflection in women compared with those in men. In addition, an inverse relationship between arterial stiffness and left ventricular diastolic function was identified in both sexes. Therefore, higher arterial stiffness may contribute to the greater risk of developing heart failure in the presence of a normal ejection fraction in women. In both men and women, there is a linear increase in arterial stiffness with aging. Although women have increased arterial stiffness, this may be somewhat tempered by female sex steroids during the reproductive years. Following menopause, there is a profound acceleration in arterial stiffening, probably ...

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Review: Sex specific programming: A critical role for the renal renin–angiotensin system

Cited by 108 publications

References 55 publications

Preterm Birth and Hypertension Risk

Preterm Birth and Hypertension Risk

Adverse prenatal environment and kidney development: implications for programing of adult disease

Sex-Related Differences in Hypertension

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