Nociceptin into the PL reduced cardiovascular responses induced by restraint stress.
NOP receptors blockade in PL potentiated pressor and tachycardiac responses induced by acute RS.
UPF-101 blocked the RS-evoked changes following nociceptin administration into the PL.
PL N/OFQ system increase cardiac parasympathetic activity during RS.
Blockade of NOP receptors in the IL did not affect the autonomic responses induced by acute RS.