The role of angiotensin II and relaxin in vascular adaptation to pregnancy

Abstract

During pregnancy, systemic and uteroplacental blood flow increase to ensure an adequate blood supply that carries oxygen and nutrients from the mother to the fetus. This results in changes to the function of the maternal cardiovascular system. There is also a pregnancy-induced vasodilation of blood vessels, which is known to have a protective effect on cardiovascular health/function. Additionally, there is evidence that the effects of maternal vascular vasodilation are maintained post-partum, which may reduce the risk of developing high blood pressure in the next pregnancy and reduce cardiovascular risk later in life. At both non-pregnant and pregnant stages, vascular endothelial cells produce a number of vasodilators and vasoconstrictors, which transduce signals to the contractile vascular smooth muscle cells to control the dilation and constriction of blood vessels. These vascular cells are also targets of other vasoactive factors, including Angiotensin II (Ang II) and relaxin. The binding of Ang II to its receptors activates different pathways to regulate the blood vessel vasoconstriction/vasodilation, and relaxin can interact with some of these pathways to induce vasodilation. Based on the available literature, this review outlines the cardiovascular changes that occur in a healthy human pregnancy, supplemented by studies in rodents. A specific focus is placed on vasodilation of blood vessels during pregnancy; the role of endothelial cells and endothelium-derived vasodilators will also be discussed. Additionally, different pathways that are activated by Ang II and relaxin that result in blood vessel dilation will also be reviewed.

Natural history of blood pressure in sickle cell disease pregnancy

“…7,15 Many cardiovascular adaptations of pregnancy are mediated by vascular signalling changes. 16,17 People with SCD have well described vascular damage and aberrant vascular responsiveness 18,19 which may limit their physiological adaptations to pregnancy. Previous studies have demonstrated abnormally low prostaglandin to thromboxane ratios during pregnancy in people with HbSS compared to unaffected pregnancies.…”

“…People with SCD, especially those with HbSS/HbSβ 0 , have high cardiac output and low systemic vascular resistance at baseline, which may limit capacity to adapt further in pregnancy 7,15 . Many cardiovascular adaptations of pregnancy are mediated by vascular signalling changes 16,17 . People with SCD have well described vascular damage and aberrant vascular responsiveness 18,19 which may limit their physiological adaptations to pregnancy.…”

The effects of systemic diseases, genetic disorders and lifestyle on keloids

“…These alterations in the wound healing process result in a disturbed mechanical status of the skin, stimulating the development of keloids with unusual characteristics and in uncommon body sites. 19,20 Pregnancy is believed to worsen pre-existing keloids or hypertrophic scars and may even trigger a previous scar to evolve into a keloid scar. 21 (Figure 3).…”

“…Skin changes involve modifications in the dermis and its vascular network, leading to an increase in the total volume of circulating blood and promoting skin inflammation. These alterations in the wound healing process result in a disturbed mechanical status of the skin, stimulating the development of keloids with unusual characteristics and in uncommon body sites 19,20 …”

“…These alterations in the wound healing process result in a disturbed mechanical status of the skin, stimulating the development of keloids with unusual characteristics and in uncommon body sites. 19 , 20 …”