**1. Introduction**

Preeclampsia is a pregnancy-specific disorder characterized by sudden onset of hypertension with either proteinuria or end-organ dysfunction, or both, after the 20th week of gestation in a previously normotensive woman, occurring in 3–5% of pregnancies in industrialized countries [1,2].

The pathogenesis of preeclampsia remains poorly understood, even though preeclampsia has been recognized for at least 100 years [3]. In the last 20 years, multiple theories about the ultimate cause of preeclampsia have been developed with little agreement, except for the conclusion that preeclampsia is a multifactorial disease [4,5].

Many approaches have been developed for predicting preeclampsia at an early stage and promising insights have been discovered [5–8]. Nevertheless, the etiology of preeclampsia remains incompletely understood, although the placenta has been identified as the central organ in the pathogenesis of preeclampsia. Impaired placentation and placental function in early pregnancy remains the leading hypothesis [9–12], while emerging hypotheses focus on the maternal cardiovascular susceptibility to preeclampsia and pregnancy adaptions [13]. Structural and functional cardiovascular changes were found in women 1 year after preeclamptic pregnancies [14], where the involvement of angiogenic factors such as soluble fms-like tyrosine kinase-1 (sFlt-1) and placental growth factor (PlGF) and placental factors such as placental protein 13 (PP13) and the dysbalance thereof may be used to predict severity and long-term cardiovascular complications of preeclampsia [15,16].

While the identification of etiological factors is without doubt an important task, the managemen<sup>t</sup> of adverse concomitant e ffects and consequences of preeclampsia may be even more relevant. Women with pregnancies complicated by preeclampsia appear to be at increased risk of metabolic and cardiovascular diseases in later life, and pregnancy complications and coronary heart disease may have common disease mechanisms [17,18]. As cardiovascular disease (CVD) is a leading cause of death, earlier recognition of those at risk seems vital. Therefore, the diagnosis of preeclampsia, or adverse pregnancy more generally, could be an opportunity for the implementation of primary prevention strategies [17,19–21].

Pregnancy is associated with huge cardiovascular and metabolic changes and can be considered as a "stress test" of the somatic and cardiovascular system, suggesting that preeclampsia manifesting in pregnancy is akin to a "failed stress test". "Failing the stress-test", that is, absence of the typical autonomically regulated cardiovascular and cardiorespiratory adaptations to pregnancy, may be predictive of cardiovascular disorders in later life, when the system is put under similar strain [21,22].

The autonomic nervous system plays a central role in cardiovascular and cardiorespiratory adaptation to pregnancy-related hemodynamic changes [23–25]. Previous research has shown that the increases in peripheral vascular resistance and blood pressure that characterize preeclampsia are mediated, at least in part, by a substantial increase in sympathetic vasoconstrictor activity [26,27]. Autonomic nervous system functioning during pregnancy can be noninvasively assessed by analyzing continuous measures of cardiovascular variables, baroreceptor reflex sensitivity (BRS), and the mutual adjustment of blood pressure, heart rate, and respiration, partitioned for influences of the sympathetic and the parasympathetic branch of the autonomic nervous system [28–31]. Now, if we can determine abnormalities in blood pressure regulation in a ffected women at a time at which their preeclampsia is no longer present by definition (i.e., from 12 weeks after delivery onwards) by use of a simple and time-e fficient test in the laboratory, this test may be used to evaluate the e ffectiveness of pharmacological or behavioral interventions for reducing a ffected women's cardiovascular risk. Therefore, the aim of this study was to follow up on the regulation of the physiological response to everyday stressful events in preeclampsia several weeks postpartum.
