Placenta

Placenta is essentially a vascular tissue but with a difference.
It has unique evolutionary behaviour with two distinct circulations one maternal and the other foetal interposed between a syncytium of trophoblastic (haemochorial) tissue which act as the inter-phase between the mother and the foetus (Beconsfield P, Birdwood G, Beconsfield R; 1996). 

The complex relationship of these circulations cannot be studied one independent of the other. When placenta separates from the basal plate at delivery only a few fragments of maternal blood vessels are left intact with the placenta. Maternal blood vessels can be studied by placental bed biopsy but the present study does not entail such an endeavour.
Broadly speaking placental development is determined by genetic, environmental, vascular and unknown factors. Genetic factors cannot be manipulated but environmental (nutrition) and vascular (pharmacological) factors are theoretically amenable to manipulation. Studies (Winick M and Noble A; 1966) have shown that in rats with intrauterine growth retardation without gross malformations there was proportionate reduction of placental weight and of protein content but had increase in RNA content. Protein / DNA ratios were normal for the size of the placenta but the RNA/DNA ratios were markedly elevated. These data indicated that in intrauterine growth retardation there was an association of reduced placental weight accompanied by reduced number of cells. The increase in RNA content was a manifested response to the placental insufficiency. For the first time their studies had shown that the small placentae of intrauterine growth retarded rats were functionally different. Whether this response is pathological or physiological was not clear from their studies but the difference of functional activity was shown. Enhanced expression of RNA may be an indication of metabolic response to stress. Whether these RNA products result in advanced placental maturation with short term survival advantage (epigenetic phenomenon) to the infant or premature expression of biological components that modify the arterial structure that leads to hypertension in adult life are contemporary issues. 

Emanuel et al  have shown increased ACTH levels in maternal blood and amniotic fluids in mothers with PIH. These findings were coincident with increased syncytial knots. Syncytial knots are not normally seen until 35 weeks of gestation and are generally considered to relate to the maturity of the placenta. In patients with PIH and placental insufficiency, an associated increased production of ACTH, an increase in number of syncytial knots and advanced placental maturation were noted by these researchers. Increased cortisol production (Lindsay RS, Lindsay RM, Edwards CRW; 1996) in placenta in intrauterine life has been associated with development of hypertension in juvenile rats.