Neurovascular dysfunctions in hypertensive disorders of pregnancy

Hypertensive disorders in pregnancy pose a huge challenge to the socioeconomic stability of a community; being a major cause of maternal and neonatal morbidity and mortality during delivery. Although there have been recent improvements in management strategies, still, the diversified nature of the underlying pathogenesis undermines their effectiveness. Generally, these disorders are categorized into two; hypertensive disorders of pregnancy with proteinuria (pre-eclampsia and eclampsia) and hypertensive disorders of pregnancy without proteinuria (gestational and chronic hypertension). Each of these conditions may present with unique characteristics that have interwoven symptoms. However, the tendency of occurrence heightens in the presence of any pre-existing life-threatening condition(s), environmental, and/or other genetic factors. Investigations into the cerebrovascular system demonstrate changes in the histoarchitectural organization of neurons, the proliferation of glial cells with an associated increase in inflammatory cytokines. These are oxidative stress indicators which impose a deteriorating impact on the structures that form the neurovascular unit and the blood-brain barrier (BBB). Such a pathologic state distorts the homeostatic supply of blood into the brain, and enhances the permeability of toxins/pathogens through a process called hyperperfusion at the BBB. Furthermore, a notable aspect of the pathogenesis of hypertensive disorders of pregnancy is endothelial dysfunction aggravated when signaling of the vasoprotective molecule, nitric oxide, amongst other neurotransmitter regulatory activities are impaired. This review aims to discuss the alterations in cerebrovascular regulation that determine the incidence of hypertension in pregnancy.