Responsiveness of Oxytocin-Producing Neurons to Acute Salt Loading in Rats: Comparisons with Vasopressin-Producing Neurons

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Abstract
Plasma oxytocin-associated neurophysin concentration ([OT-RNP]) was used to evaluate the responsiveness of oxytocinergic neurons to an acute salt load in Long-Evans (LE) rats and Brattleboro homozygous (DI) rats. This responsiveness was compared with that of vasopressinergic neurons in LE rats as indexed by plasma vasopressin-associated neurophysin concentration ([VP-RNP]). Acute salt loading was induced by infusing 18% saline for 60 min into conscious, trained, chronically catheterized animals and plasma osmolality (Posm) and mean arterial pressure (MAP) were monitored. An increase in Posm was associated with a rise in [OT-RNP] and the relationship between Δ[OT-RNP] and ΔPosm was similar for both LE and DI rats over the first 40 min of infusion (21.6 and 19.7 fmol ml–1 mosm–1 kg–1, respectively). Although Posm continued to rise between 40 and 60 min infusion, [OT-RNP] actually fell slightly during this period in LE rats to a final elevation of 682 ± 40 fmol/ml above initial values whereas [OT-RNP] in DI rats continued to rise to a final elevation of 1,927 ± 288 fmol/ml above initial values at 60 min of infusion. The differences between these elevations at 60 min for LE and DI rats were highly significant (p < 0.001). For LE rats, the increase of [OT-RNP] with Posm for the first 40 min of infusion was much greater than the increase in [VP-RNP] with the slope between Δ[VP-RNP] and ΔPosm being only 8.3 compared to 21.6 fmol ml"1 mosm–1 kg–1 in the case of Δ[OT-RNP]. This difference was significant at p < 0.002. Of some additional interest was the unexpected finding that while MAP rose gradually with infusion of hypertonic saline in LE rats, it experienced a progressive decline during infusion in DI rats. The data obtained in this study indicate that oxytocin-producing neurons release more products than vasopressin-producing neurons in response to acute increases in Posm. In addition, functioning vasopressin-producing neurons may, either directly or indirectly, have some negative feedback influence on the release of oxytocin at high plasma osmolalities (ΔPosm between + 28 and + 40 mosm/kg FLO). Finally, the data on MAP imply that vasopressin-producing neurons may have a role in the hypertension that results from acute salt intake.