Effects of glucocorticoid administration on vasopressin release during endotoxemic shock

Abstract

Glucocorticoids can reverse hemodynamic disturbances and dependence on catecholamines in septic shock. The present study was designed to assess the hypothesis that dexamethasone (DEX) through the control of nitric oxide (NO) synthesis could regulate the release of vasopressin (AVP), which plays an important role in the regulation of arterial pressure. Endotoxemic shock was induced, in male Wistar rats, by intravenous injection of 1.5 mg/kg lipopolysaccahride (LPS). The LPS administration induced a significant decrease in mean arterial pressure (MAP) with a concomitant increase in heart rate (HR) (ΔVMAP: −16.1±4.2 mmHg; ΔVHR: 47.3±8.1 bpm). An increase in plasma AVP concentration occurred and was present for two hours after LPS administration (from 2.7±0.2 to 11.1±0.9 pg/mL) returning close to basal levels thereafter and remaining unchanged until the end of the experiment. When LPS was combined with i.v. administration of low doses of DEX (0.1 and 1.0 mg/kg of body weight), we observed an attenuation in the drop of MAP (ΔVMAP: −2.2±1.9 mmHg) and a decrease in NO plasma concentration (from 1098.1±68.1 to 523.4±75.2 μM). However this attenuation in the drop of MAP was accompanied by the decrease in AVP plasma concentration (3.7±0.4 pg/mL). These data suggest that AVP does not participate of the recovery of MAP when DEX was administered in this septic shock model. Financial Support: FAPESP, CNPq, USP.