The study was undertaken to clear up the possible contribution of mitochodrial permeability to the functioning of the medullary neurons involved in the nervous cardiovascular control. In acute experiments on anaesthetized with urethane (1.7g/kg, i. p.) rats we have analyzed effects of either activating or inhibiting mitochondrial permeability transitions (MPT) in the nucleus tractus solitarius (NTS), paramedian reticular nucleus (PMn), nucleus ambiguous (AMB), lateral reticular nucleus (LRN) by injecting an inductor of MPT phenylarsine oxide (PAO, or its inhibitor melatonin, and by preliminary administrating L-arginine and melatonin prior injections of PAO. Test injections of L-arginine, a substrate for NO-synthesis, into the nuclei resulted in lowering the SAP level (70% experiments) or its elevation (30%). Injections of PAO into those nuclei resulted in a prolonged (up to 40 min) reduce in the SAP level which never restored completely and could induce a dramatic lowering of the SAP level and animal's death. Injections of an inhibitor of MPT melatonin into the medullary nuclei increased the SAP level for up to 10 min; and preliminary administration of either L-arginine or melatonin reduced negative effects of PAO injections into them. The data obtained give evidence that changes in MPT could contribute to the effects of the medullary neurons involved in the nervous control of vessels and heart.