In this study, we investigated the role of angiotensinergic neurotransmission at nucleus reticularis ventrolateralis (NRVL), and the subtype of angiotensin receptors involved, during experimental endotoxemia induced by E. coli lipopolysaccharide (LPS). In adult male Sprague-Dawley rats maintained under propofol anesthesia (30 mg/kg/h), paralyzed with pancuronium (2 mg/kg/h) and mechanically ventilated (85-95 stroke/min, 2.5-3 ml/stroke), intravenous administration of LPS (15 or 30 mg/kg) induced an immediate hypotension, followed by a rebound increase and a secondary decrease in systemic arterial pressure (SAP). LPS also reduced the power density of the very low-frequency (0-0.25 Hz) and low-frequency (0.25-0.8 Hz) components of SAP signals (Phase ¢¹), which represented the sympathetic vasomotor tone, followed by an increase (Phase ¢º) and a secondary decrease (Phase ¢»). Pretreatment with microinjection of the selective non-peptide AT1 receptor antagonist, losartan (1.6 nmol), or the selective non-peptide AT2 receptor antagonist, PD-123319 (1.6 nmol), into the bilateral NRVL significantly reduced the survival time after the induction of acute experimental endotoxemia. Both pretreatments shortened the duration of Phase ¢º and Phase ¢» in acute endotoxemia, accelerated the secondary hypotension, and excited the power density of the very low-frequency. We conclude that endogenous angiotensin ¢º at the NRVL may play a crucial role in the maintenance of SAP during acute experimental endotoxemia, possibly via an action on both AT1 and AT2 subtype receptors on the very low-frequency component of SAP spectrum.