Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “VASOPRESSIN”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,243 records · Page 69Linked to original sources
PubMed1991

Increased vasopressin immunoreactivity in the rat brain after a postmortem interval of 6 hours.

Enhanced immunocytochemical staining of vasopressin-containing neurons was observed after incubation of rat brain slices in Ringer medium for 6 h at room temperature, as compared to brain tissue fixed immediately after death. Hypothalamic vasopressin neurons in the supraoptic nucleus, the paraventricular nucleus and the suprachiasmatic nucleus stained more intensely after a postmortem interval of 6 h. Extrahypothalamic vasopressin neurons (VP) in the bed nucleus of the stria terminalis, the medial amygdala and the locus coeruleus proved to be stained as well. Extrahypothalamic VP neurons in the locus coeruleus could, until now, only be visualized after in vivo pretreatment with colchicine. In addition, staining was observed at two new sites, the dorsal raphe nucleus and the lateral septum. Staining of VP was corroborated by application of different antibodies directed against the intact vasopressin molecule as well as by antibodies directed against the other parts of the vasopressin precursor molecule, i.e. neurophysin and glycopeptide. The specificity of the VP-staining was validated by using pre-immune serum and using Brattleboro rat brain tissue, resulting in a negative staining in both cases. Furthermore, homogenated punches of the suprachiasmatic nucleus were submitted to iso-electric focussing on polyacrylamide gel, followed by press blotting and subsequent immunocytochemical staining for vasopressin. Iso-electric foccussing enabled us to characterize and quantify peptides in the suprachiasmatic nucleus. The vasopressin content increased 6 h postmortem, while c-terminal glycopeptide and neurophysin levels remained stable. Similar results were observed in the suprachiasmatic nucleus from decapitated rats whose brains were left intact in the skull for 6 h at room temperature.

Animals↗
PubMed1979

Vasopressin analogs: sedative properties and passive avoidance behavior in rats.

The effects of several types of vasopressin analogs that are considered to be resistant to some of the physiologically significant enzymatic systems were investigated utilizing rats trained in a passive avoidance task. Enhancement of avoidance latencies was observed 2, 7 and 13 days after the single learning trial when deamino-carbavasopressins, triglycyl-8-lysine-vasopressin or its des-glycinamide derivative, and deamino-D-arginine-vasopressin were given shortly after the learning trial in the dose of 1 microgram s.c. (8-L-Arginine)deamino-6-carba-vasopressin and (8-L-ornithine)deamino-6-carba-vasopressin were also active in the dose of 0.1 microgram. Lysine vasopressin and its des-glycinamide derivative failed to enhance avoidance latencies in part of the experiments if doses of 0.3--3 micrograms were administered and 7 or 13 day intervals were used between the learning and the test trials. Enhancement of avoidance latencies was also observed, if some of the peptides were injected 20 min but not 120 or 180 min before the test trial. Marked depression of exploratory behavior of rats in an open field was found after s.c. injections of low doses (1--3 micrograms kg-1) of deamino-carba-vasopressins. Higher doses (10--30 micrograms kg-1) induced sleep-like immobility not accompanied by ataxia or catalepsy.

Animals↗
PubMed1982

Vasopressin and beta-endorphin release after osmotic and non-osmotic stimuli: effect of naloxone and dexamethasone.

The purpose of this study was to determine whether or not vasopressin release in response to various stimuli in the conscious rat is controlled by endogenous opioid peptides, in particular beta-endorphin. Naloxone (1 mg.kg-1 i.m.) promoted vasopressin release in response to both an angiotensin II infusion (500 ng . kg-1 . min-1) or an isosmolar, nonhypotensive hypovolaemia achieved by polyethylene glycol injection (PEG, 20% solution i.p.); however, naloxone was without effect when vasopressin release was induced by hypertonic saline injection (2.5% solution i.p.) or a severe fall in arterial blood pressure following trimethidinium (10 mg . kg-1 i.m.) induced ganglionic blockade. Vasopressin release was accompanied by an increase in plasma beta-endorphin-like immunoreactivity (beta-EI) following an angiotensin II infusion of PEG administration, but not after hypertonic saline or trimethidinium injection. Dexamethasone pretreatment (0.5 mg . kg-1 twice i.p.) prevented the increase in plasma beta-EI following an angiotensin II infusion or PEG administration. The simultaneous angiotensin II- or PEG-induced increase in vasopressin release was unaffected or potentiated, respectively, by the glucocorticoid. In contrast, vasopressin release in response to hypertonic saline or trimethidinium injection was significantly inhibited by dexamethasone. We conclude that an inhibitory control by endogenous opiates is involved in some, but not all of the different pathways leading to vasopressin release. The results obtained do not prove but can be reconciled with the proposal that hypophyseal beta-endorphin is the compound responsible.

Animals↗
PubMed1984

GABA agonists inhibit central sodium-induced vasopressin-dependent increases in arterial pressure.

Previous studies have demonstrated that intraventricular (i.v.t.) administration of low doses of GABA agonists reduced the central pressor effects of cerebrospinal fluid (CSF) made hypertonic with sodium (Na). The following studies were designed to determine if GABA agonists acted to decrease the pressor response of Na through inhibition of the vasopressin-dependent pressor component. Following pretreatment with vascular vasopressin antagonist, the pressor response of i.v.t. administered Na was reduced approximately 60%. Hypophysectomy produced a similar reduction in the pressor response elicited by hypertonic CSF. These results indicate that vasopressin contributed to approximately 60% of the pressor response of Na. In order to generate a vasopressin-dependent pressor response, the sympathetic nervous system was eliminated with ganglionic blockade by chlorisondamine. The increase in arterial pressure produced by i.v.t. injection of hypertonic CSF was augmented after ganglionic blockade compared to untreated rats. The augmented pressor effect of i.v.t. administered Na was markedly reduced by the vascular vasopressin antagonist or by hypophysectomy. Therefore, the pressor effect of Na after ganglionic blockade was caused almost entirely by the pressor actions of arginine-vasopressin (AVP). This AVP-dependent pressor effect of i.v.t. injected Na in rats subjected to ganglionic blockade was reduced by pretreatment with 100 micrograms of GABA or 50 ng of the GABA agonist muscimol. These doses of GABA and muscimol have previously been shown to reduce the pressor response of i.v.t. administered Na in untreated rats. Thus, pretreatment with low doses of GABA agonists reduced the pressor effect of Na in part through inhibition of the vasopressin component of the pressor response. GABA pretreatment also antagonized the increase in plasma AVP levels produced by i.v.t. administered hypertonic CSF.

Animals↗
PubMed1992

Pharmacological characterization of serotonin receptor subtypes involved in vasopressin and plasma renin activity responses to serotonin agonists.

Serotonergic drugs with 5-HT2 receptor agonist properties have been suggested to increase plasma vasopressin concentration, blood pressure (BP) and plasma renin activity (PRA). To study whether these actions are mediated by the same or different receptors, we used three potent 5-HT agonists with different structures and receptor binding profiles. All drugs were administered i.v. to conscious, unrestrained rats. The selective agonist, 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI), which has high affinity for 5-HT2 receptors, caused marked increases in BP and PRA but no change in plasma vasopressin concentrations. The 5-HT1C agonist, m-chlorophenylpiperazine (m-CPP), which also binds to other 5-HT receptors, caused moderate increases in BP and PRA and significantly elevated plasma vasopressin concentrations. The 5-HT1A agonist, 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT), did not increase any of these parameters. BP and PRA elevations paralleled each other after all drugs, while vasopressin responses were clearly different. Vasopressin responses to m-CPP were entirely antagonised by the 5-HT1/5-HT2 antagonist metergoline, partially by the 5-HT2/5-HT1C antagonists ritanserin and LY 53857, but not by the 5-HT2 antagonist ketanserin. Ritanserin, LY53857 and ketanserin all very effectively blocked BP responses to m-CPP. These findings suggest that BP and PRA but not vasopressin responses are mediated by 5-HT2 receptors. Vasopressin secretion is mediated by 5-HT1 receptors, most likely by 5-HT1C receptors.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1996

Antisense oligonucleotide to c-fos blocks the ability of arginine vasopressin to maintain ethanol tolerance.

Administration of the neuropeptide, arginine vasopressin, can reduce the rate of dissipation of functional ethanol tolerance in mice that have acquired that tolerance. We previously showed that intracerebroventricular vasopressin administration can also produce an increase in septal c-fos mRNA levels. To evaluate the role of the increased expression of c-fos in the ability of vasopressin to maintain tolerance, ethanol-tolerant mice were given intracerebroventricular injections of vasopressin in the presence or absence of an antisense oligonucleotide to c-fos. The antisense oligonucleotide completely blocked the ability of vasopressin to maintain ethanol tolerance, while a missense oligonucleotide was without effect. The antisense oligonucleotide also attenuated the increase in septal c-fos mRNA levels caused by vasopressin. The results provide evidence for a role of c-fos expression in the maintenance of ethanol tolerance by vasopressin.

Analysis of Variance↗
PubMed1991

Effect of intrathoracic pressure on plasma arginine vasopressin levels.

Abdominal distention during pneumoperitoneum results in a marked increase in plasma arginine vasopressin levels, which has been ascribed to an increase in intrathoracic pressure. Because of this relationship, tense ascites could contribute to nonosmotic release of antidiuretic hormone, to the development of hyponatremia, and eventually to further ascites formation. The effect of pneumoperitoneum, thoracocentesis, and paracentesis on plasma arginine vasopressin levels was studied in three groups of patients, and the mechanism by which these maneuvers may induce these changes was investigated. Patients with pleural effusion, pneumothorax, or ascites showed a significant increase in plasma arginine vasopressin levels, and thoracocentesis or paracentesis resulted in a decrease in these levels. Plasma vasopressin levels increased significantly during pneumoperitoneum, as did intrathoracic and atrial pressures; the atrial transmural pressure gradient declined. However, no changes in plasma levels of norepinephrine, aldosterone, and renin activity were observed during pneumoperitoneum. Changes in plasma arginine vasopressin levels correlated with the changes in intrathoracic and atrial pressures and transmural pressure gradient. The authors conclude that increased intrathoracic pressure is associated with an increase in plasma arginine vasopressin levels and propose that ascites could be a factor promoting vasopressin release by acting on intrathoracic volume receptors in decompensated cirrhotics.

Adult↗
PubMed1995

A meta-analysis of somatostatin versus vasopressin in the management of acute esophageal variceal hemorrhage.

BACKGROUND & AIMS: Although sclerotherapy is the current standard therapy for bleeding esophageal varices, the best method for initial control is unclear. The aim of this meta-analysis was to compare the efficacy and toxicity of somatostatin and vasopressin in short-term treatment of hemorrhage from esophageal varices. METHODS: Using MEDLINE, all randomized trials comparing somatostatin with vasopressin in subjects with endoscopically documented acute esophageal variceal bleeding were identified. The quality of each study was critically and independently evaluated, and quantitative data for initial cessation of bleeding, sustained control of bleeding, and major adverse effects were abstracted. The relative risk (RR) and number needed to be treated were calculated. RESULTS: The RR or likelihood of achieving initial control of bleeding with somatostatin vs. vasopressin was 1.62 (95% confidence interval [CI], 1.37-1.93), and the number needed to be treated was 3.7, i.e., between 3 and 4 patients would have to be treated with somatostatin for 1 patient to derive additional benefit over vasopressin. For trials that measured sustained control of bleeding, somatostatin was superior to vasopressin (RR, 1.28 [95% CI, 1.00-1.65]; number needed to be treated, 8.8). The risk of adverse effects was greater for subjects given vasopressin (10% vs. 0%; P = 0.00007). CONCLUSIONS: This meta-analysis suggests that somatostatin is more efficacious in controlling acute hemorrhage from esophageal varices and has a lower risk of adverse effects than vasopressin.

Acute Disease↗
PubMed1996

V2-receptor blockade enhances pressor response to vasopressin: gender difference.

The present study was performed to determine if the attenuated pressor response to vasopressin in conscious non-estrous female rats is due in part to an enhanced V2-like receptor vasodilator action. In male rats, infusion of vasopressin at a rate of 1 ng.min(-1).kg body weight-1 (wt) resulted in an increase in mean arterial blood pressure (MABP) of about 20 mm Hg. Thirty minutes after beginning the infusion of vasopressin, the iv bolus injection of a non-peptide V2-receptor antagonist, OPC-31260 (2 mg.kg body wt-1), resulted in a further gradual increase in MABP of approximately 8 mm Hg in the next 60 min (p < 0.05). Thus, the pressor response to vasopressin was greater in OPC-31260-treated than in vehicle-treated male rats (p < 0.01). The pressor response to vasopressin 30 min after the start of its infusion was lower (about 8 mm Hg) in non-estrous female rats than in males. During the next 60 min of vasopressin infusion, there was a small further increase (p < 0.05) in MABP in the females given either OPC-31260 or its saline vehicle. In contrast to the male rats, however, there was no difference in MABP between the OPC-31260 and vehicle treated females. Thus, the present study has provided additional evidence for a V2-like receptor related vasodilator effect in male rats. However, since female rats do not appear to express a V2-receptor mediated vasodilator response, the sexually dimorphic pressor response to vasopressin cannot be due to a gender difference in V2-receptor vasodilator activity.

Animals↗
PubMed1983

beta-Endorphin controls vasopressin release during foot shock-induced stress in the rat.

This study tested the possibility that beta-endorphin is involved in the regulation of vasopressin release during stress induced by inescapable electric foot shock. To this end, a specific anti-beta-endorphin antiserum or a control serum lacking the specific anti-beta-endorphin antibodies was administered to male rats. Plasma vasopressin concentrations, measured by radioimmunoassay, were not affected by brief foot shock stress in control rats, but were raised significantly by the stress in animals which had received an intracerebroventricular (i.c.v.) injection of the anti-beta-endorphin antiserum. In contrast, when the same volume of the anti-beta-endorphin antiserum was injected into a tail vein, foot shock stress produced only a slight effect on vasopressin release. I.c.v. injection of the antiserum changed neither basal nociceptive threshold nor stress-induced analgesia as revealed by the tail-flick latency. Vasopressin release induced by an osmotic stimulus was not influenced by the anti-beta-endorphin antiserum given i.c.v. The opiate antagonist naloxone or the glucocorticoid dexamethasone raised plasma vasopressin concentration in stressed rats which had received the control serum (i.c.v.); however, after i.c.v. injection of the anti-beta-endorphin antiserum neither naloxone nor dexamethasone elevated the plasma vasopressin concentration beyond the level reached by the anti-beta-endorphin antiserum (i.c.v.) alone. These results suggest that beta-endorphin inhibits the release of vasopressin during foot shock-induced stress in the rat.

Animals↗
PubMed1993

Plasma concentrations of arginine vasopressin, oxytocin and angiotensin in patients with hymenoptera venom anaphylaxis.

The plasma concentrations of arginine vasopressin, oxytocin, angiotensin I and II were studied in patients with hymenoptera venom anaphylaxis (n = 50) and healthy volunteers (n = 25). There was no difference in arginine vasopressin: 5.52 +/- 0.45 fmol/ml vs. 3.99 +/- 0.41 fmol/ml or oxytocin: 28.10 +/- 1.13 fmol/ml vs. 26.24 +/- 1.80 fmol/ml between patients and controls. No correlation between the severity of clinical symptoms and the plasma levels of arginine vasopressin and oxytocin was found in patients. However, patients with a history of hymenoptera venom anaphylaxis showed significantly reduced angiotensin I and angiotensin II plasma levels as compared to controls (ANG I: 9.51 +/- 0.61 fmol/ml vs. 22.91 +/- 1.73 fmol/ml; ANG II: 2.84 +/- 0.16 fmol/ml vs. 6.95 +/- 0.33 fmol/ml). A significant inverse correlation between the severity of clinical symptoms and the plasma levels of angiotensin I and angiotensin II was observed; the lower the concentrations the more severe the clinical symptoms. Oxytocin immunoreactivity eluted from the HPLC column as a single peak with the same retention time as synthetic oxytocin. The vasopressin immunoreactive material could be characterized on HPLC as arginine-vasopressin and two other peptides of unknown nature which crossreacted with the vasopressin antibody. These findings suggest a possible role of angiotensin I and angiotensin II in hymenoptera venom anaphylaxis while arginine vasopressin and oxytocin are most likely not involved.

Adolescent↗
PubMed1989

Effect of arginine vasopressin on coronary and systemic hemodynamics in man.

Arginine vasopressin is a potent constrictor of isolated arterial segments in vitro. However, it is disputed whether, in vivo, arginine vasopressin acts as either a systemic or coronary vasoconstrictor. The purpose of this study was to determine the effect of arginine vasopressin on coronary and systemic vascular tone in man. Six patients undergoing routine diagnostic cardiac catheterization were studied. At angiography, all patients were found to have severe coronary artery disease. Cardiac and systemic pressures and coronary blood flow as well as serum arginine vasopressin and osmolality levels were measured before and after administration of hypertonic contrast dye and then following intravenous injection of an analog inhibitor of arginine vasopressin. At baseline, serum arginine vasopressin levels were within the normal range in all patients, but, following infusion of contrast dye, rose above physiological levels in 5 patients. In these latter patients, there were no significant changes in coronary and systemic hemodynamics between baseline (condition 1), following administration of contrast dye (condition 2) and 10 minutes after injection of arginine vasopressin inhibitor (condition 3). Mean coronary sinus blood flow (ml/min) and mean coronary vascular resistance (dyne.sec.cm-5) were 184 +/- 49 and 41,235 +/- 8275 during condition 1, 204 +/- 62 and 39,442 +/- 8781 during condition 2, and 192 +/- 75 and 44,930 +/- 11455 during condition 3. Mean arterial pressure (mm Hg) and mean systemic vascular resistance (dyne.sec.cm-5) during conditions 1, 2 and 3 were 105 +/- 12 and 1454 +/- 174, 114 +/- 21 and 1432 +/- 210, and 114 +/- 15 and 1436 +/- 147, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

Vasopressin administration to neonatal rats reduces antidiuretic response in adult kidneys.

Neonatal rats who had been given injections of vasopressin on days 1-7 after birth exhibited polyuria as adults. In vivo antidiuresis bioassays demonstrated that their kidneys were deficient in their ability to concentrate urine in response to stimulation with vasopressin. The kidneys also showed a reduction in vasopressin-induced cyclic AMP production, although parathyroid hormone- and calcitonin-induced levels were normal. This suggests a specific deficit in vasopressin receptor-adenylate cyclase function. In contrast, the neonatal treatment had no effect on the sensitivity of the adult vasculature to the hypertensive effects of vasopressin. These results show that short exposures to high levels of vasopressin early in development can produce a long-term defect in vasopressin responsiveness that is specific to the kidney.

Animals↗
PubMed1984

In vitro and in vivo studies on development and regeneration of vasopressin neurons.

The present paper reviews recent work conducted in our laboratory on vasopressin neurons either grown in culture or transplanted into vasopressin deficient rats. The in vitro model of reaggregated cell culture used the anterior hypothalamus, including vasopressin neurons of the SON from normal timed-pregnant LE rats of similar ages used in our in vivo model. Various cells were co-cultured with their known target tissue, the posterior pituitary to analyze further the influence of the target tissue on hormone production. At a designated end point, cultured cells were fixed and stained immunocytochemically for vasopressin and neurophysin. Radioimmunoassay of the samples was performed for vasopressin quantification. Hypothalamic cells from all ages produced vasopressin (VP). The co-culturing of hypothalamus with posterior pituitary produced a significant increase in VP. Correlative transplantation studies were conducted using timed-pregnant Long-Evans (LE) rats at various days post coitus (dpc) and neonatal tissue from 0- and 5-day old rat pups. Animals survived about 40 days then were perfused and their brains processed for vasopressin and neurophysin thick-section immunocytochemistry. The results showed that the capability for survival of younger grafts was much greater than that of older tissue. With this paper, we have shown that the reaggregation of anterior hypothalamic cells in a culture system can be used for microassay of neurosecretory activity. These data suggest a close correlation between the ability of a neuron to survive transplantation and its stage of development. With the present studies, we have shown that neurons not fully differentiated maintain a greater degree of plasticity than older tissue and are better able to survive the rigors of transplantation and that various manipulations of environmental factors have an effect on brain development at critical times.

Aging↗
PubMed1985

Vasopressin: site of behavioral action and role in human mental performance.

Diminishment of endogenous vasopressin in various brain areas (dorsal and ventral hippocampus, dorsal septum) by local application of diluted anti-vasopressin serum results in attenuation of passive avoidance behavior of rats. Both post-learning or pre-retention treatment results in impaired behavior when the anti-vasopressin serum was applied in the dorsal or ventral hippocampus, whereas only pre-retention but not post-learning application of the antiserum in the dorsal septum induced behavioral impairment. Only injection of less diluted antiserum into the lateral ventricle results in attenuation of passive avoidance behavior. These results suggest that endogenous vasopressin present in these brain sites plays a functional role in brain processes related to memory and in particular in processes involved in storage and/or retrieval of information. These findings are discussed and compared with observations of vasopressin treatment on memory functions in man. The observation that some patients with memory disorders do not respond to vasopressin treatment may be due to lesions in the anatomical sites of action of vasopressin.

Animals↗
PubMedDate not supplied

Co-existence of CRF and vasopressin immunoreactivity in parvocellular paraventricular neurons of rat hypothalamus.

New dual immunocytochemical staining procedures were used in the same tissue section to elucidate the distribution and co-existence of CRF and vasopressin in parvocellular neuronal perikarya in the paraventricular nucleus (PVN) of rat hypothalamus. CRF immunostained cells were for the most part concentrated in the medial parvocellular component of PVN. Few vasopressin-immunoreactive (ir) neurons were seen in this area in the normal and colchicine-treated animals. Vasopressin-containing neurons predominated in the magnocellular component of PVN. In the adrenalectomized and adrenalectomized-colchicine-treated animals, a dense accumulation of vasopressin-ir cells were observed in the medial parvocellular area of PVN; this region is normally vasopressin-ir poor and CRF-ir rich. The vasopressin immunostained cells appeared to have an anatomical distribution similar to that seen for CRF-containing cell bodies. Results of this study unequivocally establish the co-existence of vasopressin and CRF in the same parvocellular perikarya of PVN following pertubation of the pituitary-adrenal axis.

Animals↗
PubMed1994

Mild sustained effects of neonatal vasopressin and oxytocin treatment on brain growth and behavior of the rat.

The lasting effects of a 9-day neonatal exposure to vasopressin and oxytocin were examined in the rat to discover if peptide administration results in organizational effects. When tested in young adulthood, brain growth, not body growth, appeared to be impaired. Basal and challenge tests of urine production, carried out to see the development of the hormonal antidiuretic function of vasopressin, revealed no lasting changes, and therefore did not confirm earlier findings of an induced mild polyurea. Behavioral testing of learning by making use of a one-trail step-through paradigm with a 24-h retention trial--a test that is sensitive to vasopressin--did not show impairments. Open field tests, however, showed enhanced emotionality in the vasopressin-treated females, as well as an initially increased ambulation in the males, and increased grooming in both sexes, the latter also having been reported to be induced by vasopressin administration in the septal areas. Oxytocin treatment did not produce lasting changes. Our conclusion, therefore, is that peripherally circulating vasopressin can affect the organizational development of the rat brain. It remains to be established whether this is an effect obtained through changes in the general peripheral physiology or a reflection of plasticity phenomena at the level of central vasopressin neurotransmission.

Animals↗
PubMed1985

Vasopressin and related peptides: animal and human studies.

In animals, vasopressin and related peptides are present in specific neuronal pathways in the brain and modulate brain processes. It has been suggested that in particular memory processes, including consolidation and retrieval, short and long term memories are facilitated by vasopressin. Evidence has been presented that endogenous vasopressin is involved in these processes. But also other effects of these peptides e.g. an attenuation of acquisition of heroin self-administration have been reported. Vasopressin and related peptides have been administered to humans in a number of studies including volunteers and various patient populations with and without complaints about memory. Beneficial effects on several aspects of memory, learning, attention and concentration have been found, but not in all studies. Patients with severe deficits seem to benefit less from the peptide treatment. This may be related to the amount of brain damage. Beneficial effects of vasopressin treatment have been reported in schizophrenics and heroin addicts. In addition effects on social behavior, energy and mood of certain patients have been noted. The target patient population for vasopressin neuropeptide is thus not yet well defined. With respect to cognitive disorders, sophisticated neuropsychological test procedures, including information-processing tasks, may contribute to define such a patient population. These tasks may also be applied for treatment evaluation. It should however be kept in mind that other interesting influences of vasopressin e.g. on social behavior, mood and addictive behavior, may also appear of clinical significance. Future studies in humans may yield more detailed information in this respect.(ABSTRACT TRUNCATED AT 250 WORDS)

Amnesia↗