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

Abstract

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.