Role of vasopressin in adaptation to pregnancy in chronic hypertension

Cardiovascular system (CVS) adaptation during pregnancy involves numerous hemodynamic changes and remodeling of peripheral and central regulatory mechanisms. A decrease in blood pressure (BP) during pregnancy activates the baroreflex, leading to an increase in sympathetic tone and the synthesis and secretion of vasopressin (VP). It is well-established that VP plays a critical role in the adaptation to normotensive pregnancy, as well as in the development of primary hypertension. However, the effects of VP on neuroendocrine and autonomic adaptation of the CVS in the context of chronic hypertension during pregnancy remain insufficiently studied. This study was conducted on normotensive Wistar (WR) and spontaneously hypertensive rats (SHR) implanted with radiotelemetry devices for continuous hemodynamic measurements. BP and heart rate (HR) variability were assessed through spectral analysis, while baroreflex sensitivity (BRS) was measured using the sequence method. Plasma VP concentration was measured by ELISA, and gene expression of VP, V1aR, and V1bR was analyzed via RT-qPCR. The results indicate that non-pregnant SHR females exhibit higher gene expression of VP, V1aR, and V1bR in the paraventricular nucleus (PVN) and supraoptic nucleus (SON) compared to WR females in diestrus. Pregnant SHR females show reduced VP expression in the SON, lower plasma VP concentrations, and normalized BP during late pregnancy, but also exhibit signs of increased sympathetic cardiac stimulation (elevated HR and LF-HR), as well as activation of vagal mechanisms (increased BRS and HF-HR). In WR females, late pregnancy induces increased gene expression of VP in the PVN and SON, while changes in plasma VP levels and BP are less pronounced, as are alterations in autonomic control. These findings indicate differences in adaptation between WR and SHR females.