Envolvimento da neurotransmissão nitrérgica do núcleo leito da estria terminal (NLET) nas respostas cardiovasculares ao estresse em ratos: interação com mecanismos glutamatérgicos e noradrenérgicos locais

Abstract

The aim of the present study was to assess an interaction between nitrergic neurotransmission within the bed nucleus of the stria terminalis (BNST) with local glutamatergic and noradrenergic neurotransmissions in control of cardiovascular responses evoked by an acute session of restraint stress in rats. For this, all animals were subjected to surgical procedures for implant of bilateral guide cannulas into the BNST and a catheter into the femoral artery. Bilateral microinjection of NMDA into the BNST increased the restraint-evoked tachycardia, but whithout affecting the pressor response and the drop in tail skin temperature. Changes on blood pressure, heart rate and tail skin temperature evoked by restraint stress were recorded. The acute 30 min session of restraint stress was performed five minutes following BNST pharmacological treatments. Bilateral microinjection of NMDA into the BNST enhanced the tachycardia to restraint, but without affecting the pressor response and the drop in tail skin temperature. The effect of NMDA on restraint-evoked tachycardia was completely inhibited in animals pretreated with the selective nNOS inhibitor Nω-Propyl-L-arginine (NPLA) into the BNST. Bilateral microinjection of NOC-9 decreased the heart rate and blood pressure increases evoked by restraint stress. The effect of NOC-9 on HR, but not on blood pressure, was inhibited by BNST pretreatment with WB4101. Besides, microinjection of NPLA in animals pretreated with WB4101 into the BNST decreased the HR and blood pressure increases to restraint. Taken together, these results indicate that the inhibitory control of cardiovascular responses to stress by BNST nitrergic neurotransmission is mediated by a facilitation of local noradrenergic neurotransmission. Also, present data provide evidence of an involvement of local nNOS in facilitatory control of the NMDA receptor within the BNST.