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.
We studied the effects of chronic replacement with arginine vasopressin (AVP) or 1-desamino-D-arginine vasopressin (DDAVP), as well as acute replacement with AVP or DDAVP, on the responsiveness of oxytocin (OT) neurons as indexed by plasma oxytocin-associated neurophysin concentration [( OT-RNP]) during acute salt loading in conscious, chronically catheterized homozygous Brattleboro (DI) rats. Salt loading was carried out on days 5 and 12 of AVP (3,000 ng/day) or DDAVP (50 ng/day) treatment or 60 min after intraperitoneal injection of 1 microgram AVP or 25 ng DDAVP. All vasopressin treatments did not significantly alter the basal [OT-RNP]. In response to infusion of 18% saline, there were corresponding significant increases in plasma osmolality (Posmol) and [OT-RNP] in all animals. The increases in [OT-RNP] in vasopressin-treated DI rats were markedly reduced compared with those observed earlier for untreated DI animals despite similar rises in Posmol. The slopes of the relationship between delta [OT-RNP] and delta Posmol were 9.0 and 9.8 fmol X ml-1 X mosmol-1 X kg for chronically AVP-treated DI rats, 8.9, and 8.8 fmol X ml-1 X mosmol-1 X kg for chronically DDAVP-treated DI animals, 10.7 fmol X ml-1 X mosmol-1 X kg for acutely AVP-treated DI rats, and 8.3 fmol X ml-1 X mosmol-1 X kg for acutely DDAVP-treated animals compared with that of 34.9 fmol X ml-1 X mosmol-1 X kg for untreated DI rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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