17β-Estradiol alters the response of subfornical organ neurons that project to supraoptic nucleus to plasma angiotensin II and hypernatremia.

This study was done in urethane anesthetized, ovariectomized (OVX) female rats that were either implanted or not implanted with silastic capsules containing17β-estradiol (E2) to investigate the effect of systemic changes in E2 on the discharge rate of subfornical organ (SFO) neurons that projected to supraoptic nucleus (SON) and responded to changes in plasma levels of angiotensin II (ANG II) or hypernatremia. Extracellular single unit recordings were made from 146 histologically verified single units in SFO. Intra-carotid infusions of ANG II excited ~57% of these neurons, whereas ~23% were excited by hypertonic NaCl. Basal discharge rate of neurons excited by ANG II or hypertonic NaCl was significantly lower in OVX+E2 rats compared to OVX only animals. The response of SFO neurons antidromically activated by SON stimulation to intra-carotid injections of ANG II or hypertonic NaCl was greater in the OVX only compared to the OVX+E2 rats. Intra-carotid injections of E2 in either group attenuated not only the basal discharge of these neurons, but also their response to ANG II or hypertonic NaCl. In all cases this inhibitory effect of E2 was blocked by an intra-carotid injection of the E2 receptor antagonist ICI-182780, although ICI-182780 did not alter the neuron's response to ANG II or hypertonic NaCl. Additionally, ICI-182780 in the OVX+E2 animals significantly raised the basal discharge of SFO neurons and their response to ANG II or hypertonic NaCl. These data indicate that E2 alters the response of SFO neurons to ANG II or NaCl that project to SON, and suggest that E2 functions in the female to regulate neurohypophyseal function in response to circulating ANG II and plasma hypernatremia.