Interleukin-17 induces hypertension but does not impair cerebrovascular function in pregnant rats

Is there a role of proinflammatory cytokines on degenerin‐mediated cerebrovascular function in preeclampsia?

“…A number of studies show that proinflammatory cytokines contribute to the development of hypertension through several mechanisms including (1) maternal vascular endothelial dysfunction, (2) enhanced formation of vasoconstrictors, (3) decreased production of vasodilators, and (4) activation of the sympathetic nervous system (Cornelius, 2018; Granger et al, 2001; Matsubara et al, 2015). A small number of animal studies suggest that infusion of proinflammatory cytokines TNF‐α or IL‐17 during the last trimester of normal pregnancy is sufficient to alter CBF autoregulation (Duncan et al, 2021; Duncan, Younes, et al, 2020; Warrington et al, 2015). TNF‐α infusion into pregnant rats increased brain water content, likely a result of increased BBB permeability (Warrington et al, 2015).…”

“…A follow‐up study confirmed that the CBF autoregulation was also modestly disrupted in this model, which may have contributed to BBB disruption (Duncan, Younes, et al, 2020). Infusion of IL‐17 during the last trimester of normal pregnancy had a minor impairment of CBF autoregulation at high perfusion pressures (Duncan et al, 2021). IL‐17 elicited subtle changes in the myogenic response in cerebral arteries; maximal myogenic tone was achieved at lower intraluminal pressures, suggesting a reduced buffering capacity at the highest intraluminal pressures.…”

“…In the rodent model of placental ischemia, expression of βENaC in cerebral vessels is reduced, compared to normal pregnant animals (Ryan et al, 2011). Second, normal rodent pregnancy superimposed with elevated levels of TNF‐α or IL‐17 inhibits βENaC, and possibly ASIC2 expression, in cerebral vessels and isolated VSMCs in vitro (Duncan, Granger, et al, 2020; Duncan et al, 2021; Duncan, Younes, et al, 2020). In vitro studies suggest that these cytokines inhibit βENaC expression in VSMCs via mitogen‐activated protein kinase/c‐jun N‐terminal kinase (MAPK/JNK) pathways (Duncan, Granger, et al, 2020; Duncan, Younes, et al, 2020).…”