We examined the responses of vasopressin-neurons (VP-neurons) and oxytocin-neurons (OT-neurons) to acute salt-loading in a group of conscious rats (CON, n = 8) and rats under sodium pentobarbital (NEM, 50 mg/kg, i.p., n = 8) or urethane (URE, 1.6 g/kg, i.p. n = 8) anesthesia. Fifteen minutes following the induction of anesthesia, sodium pentobarbital produced an increase in basal plasma osmolality (Posm, 290 ± 2 to 296 ± 3 mosm/kg H2O, p < 0.007) while urethane did not change basal Posm (287 ± 2 to 289 ± 2 mosm/kg H2O). Neither anesthetic agent resulted in any significant changes in basal plasma levels of vasopressin-associated neurophysin (VP-RNP) and oxytocin-associated neurophysin (OT-RNP). In response to intravenous infusion of 18% saline, all three groups of rats had similar rises in Posm. The slopes of the relationship between the rise in plasma VP-RNP and the rise in Posm were markedly reduced in both groups of anesthetized animals compared to that observed for conscious animals (CON = 2.54 ± 0.5; NEM = 1.22 ± 0.18; URE = 1.17 ± 0.24 fmol · mH · mosm–1 · kg H2O–1 p < 0.0126). The slopes of the relationship between the rise in plasma OT-RNP and the rise in Posm were not significantly (p < 0.4478) different between the CON group and the NEM group, while the slope for the URE group was significantly (p < 0.05) smaller than that for the CON group (CON = 10.9 ± 1.5; NEM = 9.3 ± 1.5; URE = 6.3 ± 0.7 fmol · ml–1 · mosm–1 · kg H2O–1). Our data suggest that anesthesia induced by either sodium pentobarbital or urethane significantly reduces the responsiveness of VP-neurons to acute salt loading, but the responsiveness of OT-neurons is lowered by urethane only. It implies that the action of urethane on OT-neurons, and perhaps also on VP-neurons, might be mediated by a mechanism different from that of sodium pentobarbital. Barbiturates are known to reduce the activity at glutamate receptors and also to enhance the activity at γ-aminobutyric acid (GABA) receptors. GABA reportedly is involved in the osmotic release of both OT-neurons and VP-neurons. Therefore, the absence of an effect by pentobarbital on OT-neurons, in addition to its inhibitory influence on VP-neurons, suggests that GABA receptors do not play a predominant role in the actions barbiturates have on the osmotic responsiveness of VP-neurons. Our data might also imply that there is a relative scarcity of glutamate receptors on OT-neurons.

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