Contribution of the paraventricular nucleus in autonomic adjustments to heat stress

We assessed the contribution of the paraventricular nucleus (PVN) in the heat stress-mediated changes in sympathetic nerve activity and blood flow redistribution from the core to the skin surface. Renal sympathetic nerve activity (RSNA), mean arterial pressure (MAP), heart rate (HR), and body and tail temperatures were recorded in anesthetized rats after bilateral microinjection of cerebrospinal fluid (CSF), lidocaine or NG-monomethyl-L-arginine (L-NMMA) into the PVN during heat stress. Heat stress was induced by a graded increase in the temperature of a heating pad for 30 min. Heat stimulus after blockade of the PVN with lidocaine resulted in a blunted RSNA response (ΔRSNA: 117.6 ± 17.0% versus 11.3 ± 7.3%), as well as blunted MAP and HR (ΔMAP: 22 ± 2 versus -0.04 ± 7.2 mmHg; ΔHR: 93.4 ± 9.3 versus 43.4 ± 18.8 bpm). Body temperature threshold for tail vasodilation was unaffected by lidocaine treatment. The increase in RSNA, MAP and HR due to heat stress in L-NMMA-treated rats reached similar levels as CSF-treated control rats. However, a higher body temperature threshold for tail vasodilation was observed after L-NMMA injection (37.3 ± 0.1 versus 37.8 ± 0.2 °C). In conclusion, an intact PVN contributes to an increase in renal sympathetic activity provoked by heat stress, resulting in cardiovascular adjustments that influence core blood redistribution to the periphery. Furthermore, during heat stress, the effect of the PVN on cutaneous vasodilation is dependent on a nitric oxide mechanism.