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Review
. 2016 Oct;68(4):826-31.
doi: 10.1161/HYPERTENSIONAHA.116.06603. Epub 2016 Aug 22.

Developmental Programming of Hypertension: Physiological Mechanisms

John Henry Dasinger  1 , Gwendolyn K Davis  1 , Ashley D Newsome  1 , Barbara T Alexander  2
Affiliations
Review

Developmental Programming of Hypertension: Physiological Mechanisms

John Henry Dasinger et al. Hypertension. 2016 Oct.
No abstract available

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Figures

Figure
Figure
A schematic representation of the proposed pathogenesis of the developmental programming of hypertension. Numerous experimental models of developmental origins including placental insufficiency, moderate maternal protein restriction, fetal exposure to exogenous glucocorticoids, and prenatal exposure to hypoxia or nicotine program a sex difference in adult cardiovascular risk. Several studies indicate that estrogen is protective against the developmental origins of increased cardiovascular risk in female offspring in early adult life. Yet, recent studies report that protection against programmed CV risk in female offspring is lost by one year of age. Despite the method of fetal insult, common mechanistic pathways contribute to programmed CV risk. This review highlights recent advances in the developmental origins of health and disease published in Hypertension. Insight from these studies indicate the importance of the renin angiotensin and endothelin systems, sympathetic nerve activity and sex steroids in the etiology of hypertension that has its origins in early life. Early adult life (3–5 months of age), middle age (12 months of age). Abbreviations: RAS, renin angiotensin system; SNA, sympathetic nerve activity.
See this image and copyright information in PMC

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