Increased lipopolysaccharide-induced hypothermia in neurogenic hypertension is caused by reduced hypothalamic PGE 2 production and increased heat loss.

Hypertension is a prevalent disease characterized by autonomic-induced elevated and sustained blood pressure levels and abnormal body core temperature (Tb) regulation. The rationale of the present study was to find out the brain-mediated mechanisms involved in the thermoregulatory changes observed during lipopolysaccharide (LPS)-induced systemic inflammation (SI - at a septic-like model) in spontaneously hypertensive rats (SHR). We combined Tb and skin temperature (Tsk) analysis, assessed prostaglandin (PG) E levels (the proximal mediator of fever) in the anteroventral region of the hypothalamus (AVPO - an important site for Tb control), oxygen consumption, cardiovascular recordings, assays of inflammatory markers and evaluation of oxidative stress in plasma and brain of male Wistar and SHR that received LPS (1.5 mg kg ) or saline. LPS induced hypothermia followed by fever in Wistar whereas in SHR a maintained hypothermia without fever were observed. These thermoregulatory responses were associated with an increased heat loss in SHR in relation to Wistar. We measured LPS-induced increased PGE levels in the AVPO in Wistar, but not in SHR. LPS-induced drop in blood pressure was higher in SHR than in Wistar. Besides, LPS-induced plasma and brain [(regions involved in autonomic control: nucleus tractus solitarius (NTS) and rostral ventrolateral medulla (RVLM)] cytokines surges were blunted whereas oxidative stress was higher in SHR. LPS-induced SI leads to blunted cytokines surges both systemically (plasma) and centrally (NTS and RVLM) and a reduced hypothalamic PGE production which are associated with an increased hypothermia mediated by increased heat loss but not by heat production in SHR. This article is protected by copyright. All rights reserved.