Effect of anteroventral third ventricle lesions on vasopressin release by organ-cultured hypothalamo-neurohypophyseal explants.

Abstract

Rats with electrolytic lesions of the tissue surrounding the third ventricle (AV3V) of the hypothalamus exhibit hypernatremia and chronic drinking deficits in response to hypertonic NaCl. These findings are suggestive of impaired osmoreception. The organ-cultured rat hypothalamo-neurohypophyseal system (HNS) previously has been shown to release vasopressin (VP) in response to osmotic stimuli. The ventral portion of the region damaged by AV3V lesions is included in the HNS explant. Thus, these studies were initiated to evaluate the ability of HNS explants which were obtained from rats previously prepared with AV3V lesions to respond to an increase in osmolality, acetylcholine, or angiotensin II with an increase in VP release. Following electrolytic ablation of the AV3V region or sham lesions and a 2-week recovery period, HNS explants were removed from rats with sham or AV3V lesions. The explants were maintained in organ culture for 4 days. On the third day in culture, increasing the osmolality of the culture medium from 295 to 315 mosm/kg H2O by the addition of NaCl resulted in a 2.5-fold increase in VP release from the explants with sham lesions, but did not significantly alter VP release from the explants with AV3V lesions. On the subsequent day in culture, acetylcholine (10(-5) M) stimulated VP release from the explants with AV3V lesions as well as the explants with sham lesions. Angiotensin II (10-5 M) also stimulated VP release from explants obtained from rats with both AV3V and sham lesions. These data suggest that the osmoreceptors which are involved in controlling VP release from the organ cultured HNS may be located in the region of the AV3V.