Cleaved caspase-3 expression in hypothalamic magnocellular neurons may affect vasopressin secretion during experimental polymicrobial sepsis

We investigated whether the vasopressin (AVP) secretion deficiency observed during cecal ligation and puncture (CLP)-induced sepsis may be caused by apoptosis in hypothalamic magnocellular neurons. Plasma cytokines (TNF-α, IL-1β and IL-6) and nitrate levels were increased during sepsis and plasma AVP levels were higher in the early phase returning to basal levels in the late phase. Concomitantly, expression of the apoptosis effector, cleaved caspase 3, was increased in magnocellular neurons, inferring that this increase in hypothalamic neurons may be caused by cytokines and elevated nitrate levels. This in turn could compromise AVP secretion in the late phase of sepsis.

► In the late phase of sepsis there is a vasopressin secretion deficiency. ► Hypothalamic oxidative stress occurs during sepsis. ► Cleaved caspase-3 (CC3) expression increases in magnocelullar neurons. ► Apoptosis in neurons may compromise vasopressin secretion in the sepsis.