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

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 (P_osm) and mean arterial pressure (MAP) were monitored. An increase in P_osm was associated with a rise in [OT-RNP] and the relationship between Δ[OT-RNP] and ΔP_osm 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 P_osm 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 P_osm for the first 40 min of infusion was much greater than the increase in [VP-RNP] with the slope between Δ[VP-RNP] and ΔP_osm 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 P_osm. 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 (ΔP_osm 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.

Physiological and Biochemical Indices of Neurohypophyseal Function in the Aging Fischer Rat

“…Interest ingly, circulating OT levels were more profoundly affected by water deprivation than AVP levels. Similar results, however, have been reported by Cheng and North [28] who used salt loading to increase plasma osmolality. The maintenance of sta ble circulating levels of AVP means that the kidneys were ex posed to concentrations sufficient under normal conditions to increase the reuptake of water in reponse to reduced water in take.…”

Secretion of Vasopressin, Oxytocin, and Two Neurophysins from Rat Hypothalamo-Neurohypophyseal Explants in Organ Culture

“…That the change in release of both neurophysins was similar indi cates that both vasopressin and OT cell types were similarly affected by this stimulus, although release from OT neurons was greater than from AVP neurons. These data are now supported by observations in vivo [3] in which an osmotic shock increases OT more than AVP. Hypertonic NaCl, which has been shown to stimulate AVP secretion in vivo [1], failed to cause a significant increase in VP-RNP and AVP release from this system.…”

Vasopressin, oxytocin, dynorphin, enkephalin and corticotrophin‐releasing factor mRNA stimulation in the rat.

“…18 % saline (Cheng & North, 1986) can all increase plasma oxytocin concentrations, and either 2-3 days dehydration or i.P. hypertonic saline will not only cause vasopressin cells to fire phasically but also increases oxytocin cell firing rate (Brimble & Dyball, 1977;Leng & Bicknell, 1986).…”