P1-76 Programming of hypertension: associations of plasma aldosterone in adult men and women with birthweight and blood pressure

Reynolds, R.M.; Walker, B.R.; Phillips, D.I.W.; Syddall, Holly; Fraser, Robert S.; Davies, Eleanor; Connell, J

doi:10.1016/s0378-3782(07)70246-3

Cited by 11 publications

(16 citation statements)

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“…In their initial description of the "thrifty phenotype hypothesis" 3 , Barker and Hales proposed that BMI would be a possible mediator of the associations detected between low BW and adult T2D and CAD. The hypothesized primary effect of BMI was supported by evidence from both population and experimental studies linking low BW with predisposition to an increased risk of metabolic diseases such as T2D 25,26,27,28,29 , hypertension 30,31 and CAD 32 . However, in our study and in prior observational analyses, higher BW is associated with obesity (a universally recognized correlate of cardiometabolic disease) in both childhood 33,34 and adulthood 35,8 .…”

Section: Principal Findingsmentioning

confidence: 97%

Birthweight, Type 2 Diabetes and Cardiovascular Disease: Addressing the Barker Hypothesis with Mendelian randomization

Zanetti

Tikkanen

Gustafsson

et al. 2017

Preprint

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Section: Principal Findingsmentioning

confidence: 97%

Birthweight, Type 2 Diabetes and Cardiovascular Disease: Addressing the Barker Hypothesis with Mendelian randomization

Zanetti

Tikkanen

Gustafsson

et al. 2017

Preprint

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“…For example, maternal low-protein rat offspring have elevated circulating aldosterone levels by 4 wk of age (416). In an adult population from Hertfordshire, UK, adrenocorticotropic hormone (ACTH) stimulated aldosterone responses and blood pressure that were negatively correlated with birth weight (324). The following section reviews evidence for the role of RAS in the renal programming of hypertension.…”

Section: Renal Rasmentioning

confidence: 99%

In Utero Origins of Hypertension: Mechanisms and Targets for Therapy

Morton

Cooke

Davidge³

2016

Physiological Reviews

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The developmental origins of health and disease theory is based on evidence that a suboptimal environment during fetal and neonatal development can significantly impact the evolution of adult-onset disease. Abundant evidence exists that a compromised prenatal (and early postnatal) environment leads to an increased risk of hypertension later in life. Hypertension is a silent, chronic, and progressive disease defined by elevated blood pressure (>140/90 mmHg) and is strongly correlated with cardiovascular morbidity/mortality. The pathophysiological mechanisms, however, are complex and poorly understood, and hypertension continues to be one of the most resilient health problems in modern society. Research into the programming of hypertension has proposed pharmacological treatment strategies to reverse and/or prevent disease. In addition, modifications to the lifestyle of pregnant women might impart far-reaching benefits to the health of their children. As more information is discovered, more successful management of hypertension can be expected to follow; however, while pregnancy complications such as fetal growth restriction, preeclampsia, preterm birth, etc., continue to occur, their offspring will be at increased risk for hypertension. This article reviews the current knowledge surrounding the developmental origins of hypertension, with a focus on mechanistic pathways and targets for therapeutic and pharmacologic interventions.

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“…In a recent cross-sectional evaluation of 283 older, adult subjects with and without a history of hypertension, there were significant correlations between systolic blood pressure and levels of plasma aldosterone following suppression with dexamethasone and after stimulation with corticotropin (8). Diastolic blood pressure levels was significantly correlated with plasma aldosterone after dexamethasone administration.…”

Section: Aldosterone and Hypertensionmentioning

confidence: 99%

The Role of Aldosteronism in Causing Obesity-Related Cardiovascular Risk

Calhoun

Sharma²

2010

Cardiology Clinics

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SynopsisA large body of evidence strongly links aldosterone to development and progression of cardiovacscular disease, including vascular stiffness, left ventricular hypertrophy, congestive heart failure, chronic kidney disease, and especially, hypertension. Emerging data suggests that adipocytes may serve as a source of aldosterone, either directly, or indirectly, through release of aldosteronestimulating factors. If adipocytes are confirmed to contribute importantly to hyperaldosteronism, it would have significant clinical implications in linking aldosterone to obesity-related increases in cardiovascular risk. Such a cause-and-effect would then provide the opportunity to reverse that risk with preferential use of aldosterone antagonists in obese patients.

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P1-76 Programming of hypertension: associations of plasma aldosterone in adult men and women with birthweight and blood pressure

Cited by 11 publications

References 0 publications

Birthweight, Type 2 Diabetes and Cardiovascular Disease: Addressing the Barker Hypothesis with Mendelian randomization

Birthweight, Type 2 Diabetes and Cardiovascular Disease: Addressing the Barker Hypothesis with Mendelian randomization

In Utero Origins of Hypertension: Mechanisms and Targets for Therapy

The Role of Aldosteronism in Causing Obesity-Related Cardiovascular Risk

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