Angiotensinergic pathway through the median preoptic nucleus in the control of oxytocin secretion and water and sodium intake.

Our objective was to study in which situations the median preoptic nucleus (MnPO) interferes with the control of oxytocin secretion and salt intake and the possible mediation of angiotensin II (AII) through their AT1 receptors. Lesion of the MnPO by ibotenic acid in male rats did not change water and NaCl intake in conditions of ad libitum offer, water deprivation or salt load, but it did cause significant decrease of NaCl intake in sodium depleted animals. These animals presented higher water intake or lower NaCl intake after microinjection of AII or losartan into the MnPO, respectively. They decreased plasma oxytocin after microinjection of losartan into the MnPO, but not of AII or isotonic saline. Oxytocin secretion induced by hypertonic saline i.p. was reduced by microinjection of AII, but not losartan into the MnPO. On the other hand, microinjection of losartan in this area, but not AII, reduced plasma oxytocin in animals submitted to the isotonic saline i.p. Thus, it seems that the sodium intake control is performed by MnPO neurons through the stimulatory action of angiotensin II on AT1 receptors under sodium depletion, but not water deprivation or salt overload neither of ad libitum water and salt intake condition. On the other hand, in the high-sodium condition, endogenous angiotensin did not act on MnPO neurons to the control of oxytocin secretion while exogenous angiotensin inhibited oxytocin secretion. These results indicate two possible angiotensinergic neural circuits: one is stimulating and the other is inhibiting oxytocin secretion, depending on sodium balance.