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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Peripheral administration of vasopressin (VP) was previously shown to exert a negative feedback influence on its own release and on the release of oxytocin (OT). In this study we examined the possible influence that OT has on the function of hypothalamic magnocellular neurones. Oxytocin was administered intraperitoneally and its effects on release from VP neurones and from OT neurones were determined as indexed by plasma concentrations of vasopressin-associated neurophysin ([VP-RNP]) and oxytocin-associated neurophysin ([OT-RNP]) under basal conditions and conditions of high plasma osmolality (Posm) induced by acute salt loading. Studies were performed on conscious, chronically instrumented Long-Evans rats. Oxytocin (1 nmol or 10 nmol) dissolved in 1 mL of 0.9% saline was administered intraperitoneally to animals 1 h before they received an intravenous infusion of hypertonic saline over 60 min at a rate designed to raise Posm by approximately 0.75 mosmol.min-1. Intraperitoneal injection of vehicle or 1 nmol of OT did not significantly alter [VP-RNP], [OT-RNP], or basal Posm. Administration of 10 nmol OT also had no effect on [VP-RNP] or [OT-RNP], but this dose of peptide significantly lowered basal Posm (299 +/- 2 to 290 +/- 2 mosmol/kg H2O, p less than 0.001). Both doses of OT did not significantly alter the responsiveness of VP neurones to hyperosmotic stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Absence of negative feedback by oxytocin on release from magnocellular neurones in conscious rats. 158 42

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 less than 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.ml-1.mosm-1.kg H2O-1 p less than 0.0126). The slopes of the relationship between the rise in plasma OT-RNP and the rise in Posm were not significantly (p less than 0.4478) different between the CON group and the NEM group, while the slope for the URE group was significantly (p less than 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).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Influence of pentobarbital and urethane on release from magnocellular neurons. 174 63

The present investigation examined the distributions of immunoreactive neurotensin (NT), cholecystokinin octapeptide (CCK), substance P (SP), methionine enkephalin (ENK), vasoactive intestinal polypeptide (VIP), somatostatin (SS), rat neurophysin II (RNP II), vasopressin (VP), oxytocin (OXY), tyrosine hydroxylase (TH), and serotonin in the parabrachial nuclear complex (PB) of the rat. All of these substances were localized to the PB and they appeared to be chemoarchitecturally organized within the complex. The lateral subdivision (PBL) was organized medial-lateral and ventral-dorsal. Specifically NT, CCK, and SP immunoreactive fibers were found to be the most dense in the ventral aspect of the PBL. The distribution of NT-containing fibers was similar to the pattern of CCK-containing fibers and these were localized primarily to the central zone of the PBL. Immunoreactive SP fibers and cells were found in the external and internal zones ventrally and surrounding the dorsal and dorsolateral nuclei in the PBL. Somatostatin, ENK and VIP were found to be the most dense in the dorsal PBL. Serotonin- and TH-containing cells and fibers were found in both the PBL and PBM. These results, coupled with the observations of neuronal connections of the PB and the known functions of this region, underscore the potential involvement for these neuropeptides and monoamines in limbic-brainstem mechanisms of autonomic control.
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PMID:Neuropeptide and monoamine components of the parabrachial pontine complex. 288 46

The effects of acute infusion of lithium chloride (LiCl) were studied on mean arterial pressure (MAP) and magnocellular activity as shown by the concentrations of vasopressin-associated neurophysin ([VP-RNP]) and concentrations of oxytocin-associated neurophysin ([OT-RNP]) in plasma in conscious Long-Evans rats. Chronically-cannulated rats were infused intravenously at 10 microliter/100 g body wt/min with 13% LiCl for 20 min (total dose = 6.16 mequiv./kg body wt) or 0.65% LiCl for 60 min (total dose = 0.92 mequiv./kg body wt). Effects of 13% LiCl on mean arterial pressure were also examined in vasopressin-deficient homozygous Brattleboro rats. For Long-Evans rats, infusion of 13% LiCl produced rapid and significant (P less than 0.001) increases in mean arterial pressure, the concentration of lithium in plasma ([Li+]), plasma osmolality (Posmol), [VP-RNP], [OT-RNP] and significant decreases in heart rate and sodium concentration in plasma ([Na+]). For similar changes in plasma osmolality, lithium had a greater effect than sodium on mean arterial pressure, [VP-RNP], [OT-RNP]. For the 20 min infusion of 13% LiCl, there was a significant relationship (P less than 0.033) between delta MAP and log delta[VP-RNP] with a slope of 11.9 mmHg fmol-1 ml-1 (r = 0.5678). Unlike that of Long-Evans rats, infusion of 13% LiCl only did not produce significant changes of mean arterial pressure in Brattleboro rats. For Long-Evans rats, infusion of 0.65% LiCl resulted in more gradual and smaller elevations of blood pressure, [Li+] and smaller decreases in heart rate with no significant changes in plasma osmolality, [Na+], [VP-RNP] and [OT-RNP].(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Acute infusion of lithium chloride raises blood pressure in the conscious rat. 302 62

Intraperitoneal injections of lithium chloride (LiCl) were found to increase the activity of vasopressin-neurons and oxytocin-neurons as indexed by rises in plasma concentrations of vasopressin-associated neurophysin (VP-RNP) and oxytocin-associated neurophysin (OT-RNP). Plasma VP-RNP increased 12 and 4 times basal levels (greater than or equal to 20 fmol/ml) reaching values of 248 +/- 37 fmol/ml (3.0 mEq LiCl/kg body weight) and 89 +/- 10 fmol/ml (1.5 mEq LiCl/kg body weight) at 60 minutes. OT-RNP rose to 37-and 10-times basal levels (greater than or equal to 20 fmol/ml) with peak values of 749 +/- 100 fmol/ml and 188 +/- 48 fmol/ml ten minutes following injection of 3.0 or 1.5 mEq LiCl/kg body weight. Mean arterial pressure increased in response to lithium treatment by 31 +/- 6 mm Hg at 60 minutes in rats receiving 3.0 mEq LiCl/kg and by 22.5 +/- 5 mm Hg at 10 minutes in rats receiving 1.5 mEq LiCl/kg over pretreatment values (125 +/- 3 mm Hg). Heart rate decreased from a pretreatment value of 422 +/- 12 beats/min to 367 +/- 48 beats/min at 10 minutes and to 341 +/- 27 beats/min at 20 minutes for rats treated with the high and low dose of lithium, respectively. These findings suggest that the behavioral effects of LiCl could result from multiple mechanisms and involve its acute release of vasopressin and oxytocin. It is also possible that changes in cardiovascular function may act as cues when LiCl is used as an aversive stimulus.
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PMID:Effects of intraperitoneal injection of lithium chloride on neurohypophyseal activity: implications for behavioral studies. 303 54

Heterozygous Brattleboro (HZ) rats exhibit a partial genetic deficiency in hypothalamic vasopressin (VP) production. The effects of this abnormality of HZ rats on the capacities of VP-neurons and oxytocin (OT)-neurons to respond to an acute salt-load were examined. Acute salt-loading was induced by intravenous infusion of 18% saline in conscious, chronically catheterized animals and the activities of VP-neurons and OT-neurons were interpreted from plasma concentrations of VP-associated neurophysin, [VP-RNP] and OT-associated neurophysin, [OT-RNP] at different time periods throughout the infusion. Plasma sodium concentration ([Na+]), plasma osmolality (Posm) and mean arterial pressure (MAP) were also monitored. Salt-loading produced significant rises in [VP-RNP] and [OT-RNP]. These rises were accompanied by increases in plasma [Na+], Posm and MAP. Releases of OT-RNP were approximately four times greater than those of VP-RNP. The responsiveness of VP-neurons to increases in Posm in the HZ rat was approximately one-half of that observed for the Long-Evans (LE) rat. Furthermore, the responsiveness of OT-neurons in these animals was approximately one-half of that for LE rats and one-third of that for homozygous Brattleboro (DI) rats. The changes in MAP during salt-loading do not appear to be different for HZ and LE rats. Hence, while VP may be involved in the rise in blood pressure during infusion of hypertonic saline, there is not a direct correlation between plasma levels of VP-RNP (and presumably VP) and rises in blood pressure.
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PMID:Reduced responsiveness to acute salt-loading of vasopressin-neurons and oxytocin-neurons in the heterozygous Brattleboro rat. 357 2

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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PMID:Exogenous vasopressin modulates activity of oxytocin neurons in homozygous Brattleboro rats. 377 64

We studied the responses of the hypothalamo-neurohypophysial system to intravenous infusions of 18% saline, 25% mannitol and a combination of 15% mannitol and 1.35% saline in conscious, chronically catheterized Long-Evans rats. Infusions of 18% saline and 25% mannitol produced similar increases in plasma osmolality (Posm) and plasma vasopressin-associated neurophysin concentration [( VP-RNP]). As expected, plasma sodium concentration [( Na+]) for the 18% saline-treated animals was significantly elevated while that for the 25% mannitol-treated animals was significantly reduced. Mannitol infusion caused a significantly greater loss of body weight. The slopes of the relationship between delta [VP-RNP] and delta Posm were almost identical for the two groups. Infusion of a combination of 15% mannitol and 1.35% saline produced a rise in Posm comparable to that observed for the other two infusion regimens, but caused smaller increases in [VP-RNP], the slope of the relationship between delta [VP-RNP] and delta Posm being about half of those for the infusion with 18% saline or 25% mannitol. This combination also maintained [Na+] close to normal levels and in these animals there was a loss of body weight that was significantly smaller than that for those rats receiving 25% mannitol. The results of this study imply that factors other than osmoreceptors and/or sodium receptors are involved in causing a release of neurohypophysial principles during acute infusion of hypertonic solutions.
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PMID:Effects of acute increases in plasma osmolality on plasma vasopressin-associated neurophysin in conscious rats: implications for osmoregulation. 392 63

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 delta [OT-RNP] and delta Posm 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 less than 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 delta [VP-RNP] and delta Posm being only 8.3 compared to 21.6 fmol ml-1 mosm-1 kg-1 in the case of delta [OT-RNP].(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Responsiveness of oxytocin-producing neurons to acute salt loading in rats: comparisons with vasopressin-producing neurons. 395 71

The responses of vasopressinergic neurons to acute salt loading and to graded hemorrhage were studied in rats under conscious and anesthetized conditions. Chronically cannulated rats were used in this study so that pre- and postanesthetic conditions could be studied in the same animals. Anesthesia induced by a combination of ketamine hydrochloride and pentobarbital sodium (Nembutal) did not cause a release of vasopressin-associated neurophysin (VP-RNP). In response to infusion of 18% saline, animals in the anesthetized state had significantly greater increases in plasma osmolality (Posmol) and plasma sodium concentration than animals in the conscious state. However, the rate of increase in plasma VP-RNP concentration ([VP-RNP]) as well as the relationship between [VP-RNP] and Posmol were not significantly different for the two states. Graded hemorrhage caused similar rates of increase in [VP-RNP] for animals under conscious and anesthetized conditions. These data suggest that anesthesia induced by ketamine plus pentobarbital sodium does not change the responsiveness of vasopressinergic neurons to acute salt loading and to graded hemorrhage.
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PMID:Function of vasopressinergic neurons in rats under conscious and anesthetized conditions. 397 Jan 92


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