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Review
. 2020 Sep:224:115-123.e2.
doi: 10.1016/j.jpeds.2020.05.028. Epub 2020 May 22.

Fetal Growth Restriction and Hypertension in the Offspring: Mechanistic Links and Therapeutic Directions

Arvind Sehgal  1 , Barbara T Alexander  2 , Janna L Morrison  3 , Andrew M South  4
Affiliations
Review

Fetal Growth Restriction and Hypertension in the Offspring: Mechanistic Links and Therapeutic Directions

Arvind Sehgal et al. J Pediatr. 2020 Sep.
No abstract available

Keywords: ACE2; angiotensin-(1-7); cardiovascular disease; developmental origins of health and disease; fetal growth restriction; programming; renin-angiotensin system; vascular ageing.

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Figures

Figure 1.
Figure 1.
Mechanisms involved in increased arterial thickness and stiffness (central role of the RAS). ACE2, angiotensin-converting enzyme 2; Ang-(1–7), angiotensin-(1–7); AT1R, angiotensin II type 1 receptor; MasR, Mas receptor; NO, nitric oxide; TGF, transforming growth factor.
Figure 2.
Figure 2.
There is no change in blood flow to the brain or heart but an increase in blood flow to the adrenal glands in the chronically hypoxemic intrauterine growth restriction (IUGR) (black bars) compared with the control (white bars) fetus, A. However, there is a decrease in oxygen and glucose delivery to the heart of the IUGR fetus compared with controls, B and C.
Figure 3.
Figure 3.
Summary of therapeutic constructs. Ang, angiotensin; SNS, sympathetic nervous system; PNS, parasympathetic nervous system.
See this image and copyright information in PMC

Comment in

  • Fetal growth restriction, nutrition, and the renin-angiotensin system.
    Arisaka O, Ichikawa G, Koyama S, Sairenchi T. Arisaka O, et al. J Pediatr. 2021 Mar;230:274-275. doi: 10.1016/j.jpeds.2020.11.044. Epub 2020 Nov 26. J Pediatr. 2021. PMID: 33249007 No abstract available.
  • Reply.
    South AM, Alexander BT, Morrison JL, Sehgal A. South AM, et al. J Pediatr. 2021 Mar;230:275-276. doi: 10.1016/j.jpeds.2020.11.051. Epub 2020 Nov 27. J Pediatr. 2021. PMID: 33253734 No abstract available.

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