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PubMed1986

A quantitative analysis of the interrelationships between subpopulations of rat sensory neurons containing arginine vasopressin or oxytocin and those containing substance P, fluoride-resistant acid phosphatase or neurofilament protein.

In rat L5 dorsal root ganglia 50% of neurons contained arginine vasopressin-like immunoreactivity and 38% oxytocin-like immunoreactivity, the oxytocin entirely coexisting with the arginine vasopressin. Staining of alternate mirror-image sections with RT97 (an antibody to neurofilament protein, and a marker for large light neurons) and with arginine vasopressin antiserum showed that the two were entirely complementary, thus establishing arginine vasopressin as a marker for all small dark neurons. Mirror-image staining also showed that neurons containing substance P-like immunoreactivity and those containing fluoride-resistant acid phosphatase activity were each contained within the arginine vasopressin-positive population. Arginine vasopressin-like immunoreactivity was axonally transported in the dorsal root and (in greater quantity) in sciatic nerve. Arginine vasopressin-like immunoreactivity was present also in laminae I and II of the dorsal horn of the spinal cord and this reactivity was absent in animals which had been treated neonatally with capsaicin, suggesting that it was contained in primary afferent terminals. These results are discussed in terms of their implications for the classification of primary afferent neurons and of a possible physiological role for arginine vasopressin in these neurons.

Acid Phosphatase↗
PubMed1989

Vasopressin immunoreactivity in the anterior hypothalamus is altered during the establishment of dominant/subordinate relationships between hamsters.

When paired for 15-min periods for 5-8 consecutive days, castrated, testosterone-treated hamsters consistently assumed the dominant status, based on a higher aggression index (18 +/- 3) and frequency of flank marking (15 +/- 3) as compared to their castrated, untreated subordinate partners (-1.3 +/- 1 and 2.4 +/- 1, respectively). In addition to these hamsters with established dominant/subordinate relationships, control hamsters with no social interactions were killed, and in all animals the vasopressin level in the anterior hypothalamus-medial preoptic area was assessed by counting vasopressin immunoreactive perikarya following immunocytochemistry, or by radioimmunoassay of vasopressin from tissue punches. In the socialized pairs the subordinate hamsters had a significantly (P less than 0.01) lower number of vasopressin staining perikarya in the anterior hypothalamus, specifically the area of the nucleus circularis, than their dominant partners (n = 6 pairs). There was also a significantly (P less than 0.001) lower level of vasopressin immunoreactivity in punches taken from the area of the nucleus circularis in subordinate hamsters as compared to their dominant partners (n = 14 pairs). However, there were no significant differences in the number of perikarya or the concentration of immunoreactive vasopressin between subordinate and dominant hamsters in the supraoptic nucleus, paraventricular nucleus, suprachiasmatic nucleus or bed nucleus of the stria terminalis. The number of perikarya (n = 5 pairs) and concentration of vasopressin (n = 8 pairs) for all vasopressin immunoreactive sites, including the nucleus circularis, were similar for testosterone-treated and untreated hamsters that remained isolated and not subjected to daily aggressive encounters.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Expression of c-fos in restricted areas of the basal forebrain and brainstem following single or combined intraventricular infusions of vasopressin and corticotropin-releasing factor.

Vasopressin has been shown to be localized in specific central nervous system (CNS) sites. There is considerable evidence that it can act as a central neurotransmitter and it has been ascribed a variety of putative roles in the CNS. To identify those regions of the brain capable of responding to this peptide, 250 pmol vasopressin were infused into the lateral ventricle intracerebroventricular of conscious, handled male rats, and their brains processed for fos-immunohistochemistry 60 min later. Increases in fos-immunoreactivity, compared with cerebrospinal fluid-infused controls, were found in specific regions of the basal forebrain and brainstem: the central nucleus of the amygdala, ventrolateral septum, parvocellular divisions of the paraventricular nucleus of the hypothalamus, dorsal tuberal nucleus and locus coeruleus. Pre-infusion of 2500 pmol of a V1a antagonist prevented or reduced the expression of c-fos by intracerebroventricular vasopressin in all areas except the dorsal parvocellular paraventricular nucleus, implying that in most (but not all) areas the actions of vasopressin are mediated by the V1a receptor. Central administration of vasopressin had no effect on plasma corticosterone levels. Vasopressin and corticotropin-releasing factor act synergistically on the anterior pituitary to cause release of adrenocorticotropic releasing hormone and have corresponding synergistic interactions on behaviour. Infusion of 250 pmol corticotropin releasing factor produced a similar but not identical pattern of fos-like immunoreactivity to that of vasopressin. Activation of the parabrachial nucleus was observed, but there was no significant effect on the lateral septum and apparent increases in the medial parvocellular division of the paraventricular nucleus and locus coeruleus were not significant. Corticotropin releasing factor also caused a marked rise in plasma corticosterone. When the two peptides were infused together (125 pmol each) no evidence for synergy was found, in terms of the number of neurons activated to express c-fos. The induction of differential patterns of fos-like immunoreactivity by vasopressin and corticotropin-releasing factor in specific regions of the limbic forebrain and brainstem has implications for the individual roles they play in the CNS.

Animals↗
PubMed1990

Hypothalamic vasopressin mRNA levels in mice are decreased after chronic ethanol ingestion.

Vasopressin mRNA levels in the supraoptic and paraventricular nuclei of the hypothalamus, measured by in situ hybridization with a 35S-labeled RNA probe, were decreased by nearly 50% in C57BL/6NCR mice that had ingested an ethanol-containing diet for 7 days, and were tolerant to and physically dependent on ethanol. At 24 h after withdrawal, vasopressin mRNA levels in the supraoptic nucleus were still decreased, while levels in the paraventricular nucleus returned toward control values. Although plasma osmolality was increased in ethanol-fed mice, there was no increase in plasma vasopressin levels, possibly as a result of the effect of chronic ethanol ingestion to decrease vasopressin synthesis. In contrast, in mice that were dehydrated, but not fed ethanol, plasma osmolality, plasma vasopressin levels, and hypothalamic vasopressin mRNA all increased, as expected. The data suggest that chronic ethanol ingestion interferes with the synthesis and secretion of vasopressin, and may result in the reduced ability of an individual to respond to physiological stimuli for vasopressin secretion.

Animals↗
PubMed1994

Distribution and developmental change of vasopressin V1A and V2 receptor mRNA in rats.

With the reverse transcription-polymerase chain reaction (RT-PCR) method, we examined the tissue distribution of vasopressin V1A and V2 receptor transcripts in newborn and adult rats. In adult rats, vasopressin V1A receptor mRNA was detected in the brain, lung, liver and kidney, whereas vasopressin V2 receptor mRNA was found only in the kidney. In newborn rats, vasopressin V1A receptor mRNA was detected in the brain, liver, heart and kidney, whereas vasopressin V2 receptor mRNA in the kidney and brain. In the newborn rat brain the level of vasopressin V2 receptor mRNA decreased with age, and could not be detected in rats older than 2 weeks. Our results first demonstrated the extrarenal expression of vasopressin V2 receptor in the newborn rat brain. Also, the study showed that expressions of vasopressin V1A and V2 receptor mRNA transcripts are dynamically altered in the process of development.

Age Factors↗
PubMed2006

Usefulness of vasopressin administered with epinephrine during out-of-hospital cardiac arrest.

Vasopressin administration has been suggested during cardiopulmonary resuscitation, and a previous clinical trial has suggested that vasopressin is most effective when administered with epinephrine. Adult subjects (n = 325) who received > or =1 dose of intravenous epinephrine during cardiopulmonary resuscitation for nontraumatic, out-of-hospital cardiac arrest were randomly assigned to receive 40 IU of vasopressin (n = 167) or placebo (n = 158) as soon as possible after the first dose of epinephrine. The rate of return of pulses was similar between the vasopressin and placebo groups (31% vs 30%), as was the presence of pulses at the emergency department (19% vs 23%). No subgroup appeared to be differentially affected, and no effect of vasopressin was evident after adjustment for other clinical variables. Additional open-label vasopressin was administered by a physician after the study drug for 19 subjects in the placebo group and 27 subjects in the vasopressin group. Results were similar if these subjects were excluded or were assigned to an actual drug received. Survival duration for subjects admitted to the hospital did not differ between groups. In conclusion, vasopressin administered with epinephrine does not increase the rate of return of spontaneous circulation.

Aged↗
PubMed2006

Comparative hemodynamic effects of vasopressin and norepinephrine after milrinone-induced hypotension in off-pump coronary artery bypass surgical patients.

OBJECTIVE: Phosphodiesterase inhibitor is essential to the pharmacologic management of decompensated heart failure because it increases contractility and decreases afterload of right ventricle. It also improves hemodynamics and increases blood flow of the grafted internal mammary arteries and middle cerebral arteries during coronary artery bypass surgery. However, it induces vasodilation and necessitates the use of vasoconstrictors, such as norepinephrine. We hypothesized that vasopressin could recover hypotension induced by milrinone with less effect on pulmonary vascular resistance (PVR) compared to norepinephrine. METHODS: Fifty patients, undergoing coronary artery bypass graft (CABG) surgery, were assigned randomly in a double-blind manner to receive either vasopressin or norepinephrine. After baseline hemodynamic measurements, a loading dose of milrinone 50 microg/kg was infused slowly for 20 min followed by continuous infusion of 0.5 microg/(kg min). Immediately after the loading dose of milrinone, hemodynamic variables were measured, and vasopressin (VP group) or norepinephrine (NE groups) was infused. After being titrated until the mean arterial pressure was increased by 20%, hemodynamic variables were measured again. RESULTS: Milrinone infusion reduced both systemic vascular resistance (SVR, 1218+/-299 dynes/cm5 vs 838+/-209 dynes/cm5, 1345+/-299 dynes/cm5 vs 1011+/-195 dynes/cm5) and PVR (95+/-34 dynes/cm5 vs 72+/-30 dynes/cm5, 119+/-85 dynes/cm5 vs 87+/-33 dynes/cm5) in the VP and NE groups, respectively. Vasopressin and norepinephrine infusion increased both SVR (838+/-209 dynes/cm5 vs 1100+/-244 dynes/cm5, 1011+/-195 dynes/cm5 vs 1446+/-681 dynes/cm5, respectively) and PVR (72+/-30 dynes/cm5 vs 84+/-18 dynes/cm5, 87+/-33 dynes/cm5 vs 139+/-97 dynes/cm5, respectively). The PRV/SVR ratio was decreased after vasopressin infusion (0.10+/-0.03 vs 0.08+/-0.03), while no changes were found after norepinephrine infusion (0.09+/-0.02 vs 0.09+/-0.02). CONCLUSIONS: In the patients undergoing CABG surgery, both norepinephrine and low dose vasopressin were effective in restoring milrinone-induced decrease of SVR. However, only low-dose vasopressin decreased the PVR/SVR ratio that was increased by milrinone. Considering the importance of maintaining systemic perfusion pressure as well as reducing right heart afterload, milrinone-vasopressin may provide better hemodynamics than milrinone-norephinephrine during the management of right heart failure.

Aged↗
PubMed2005

Amygdalar vasopressin mRNA increases in acute cocaine withdrawal: evidence for opioid receptor modulation.

In humans, stress is recognized as a major factor contributing to relapse to drug abuse in abstinent individuals; drugs of abuse themselves or withdrawal from such drugs act as stressors. In the animals, evidence suggests that centrally released arginine vasopressin in both amygdala and hypothalamus plays an important role in stress-related anxiogenic behaviors. The stress responsive hypothalamic-pituitary-adrenal axis is under tonic inhibition via endogenous opioids, and cocaine withdrawal stimulates hypothalamic-pituitary-adrenal activity. The present studies were undertaken to determine whether: (1) 14-day (chronic) "binge" pattern cocaine administration (45 mg/kg/day) or its withdrawal for 3 h (acute), 1 day (subacute) or 10 days (chronic) alters arginine vasopressin mRNA levels in amygdala or hypothalamus; (2) the opioid receptor antagonist naloxone (1mg/kg) alters arginine vasopressin mRNA or hypothalamic-pituitary-adrenal hormonal responses in acute cocaine withdrawal; and (3) there are associated changes of mu opioid receptor or proopiomelanocortin mRNA levels. In amygdala, arginine vasopressin mRNA levels were unchanged after chronic "binge" cocaine, but were increased during acute cocaine withdrawal. Naloxone completely blocked this increase. Neither chronic cocaine nor its acute withdrawal altered amygdalar mu opioid receptor mRNA levels. The increase in amygdalar arginine vasopressin mRNA levels was still observed after subacute withdrawal, but not after chronic withdrawal. Although hypothalamic-pituitary-adrenal tolerance developed with chronic "binge" cocaine, there were modestly elevated plasma adrenocorticotropin hormone levels during acute withdrawal. While naloxone produced modest adrenocorticotropin hormone elevations in cocaine-naïve rats, naloxone failed to elicit an adrenocorticotropin hormone response in cocaine-withdrawn rats. In hypothalamus, neither chronic cocaine nor acute withdrawal altered arginine vasopressin, proopiomelanocortin or mu opioid receptor mRNA levels. These results show that: (1) opioid receptors mediate increased amygdalar arginine vasopressin gene expression during acute cocaine withdrawal, and (2) cocaine withdrawal renders the hypothalamic-pituitary-adrenal axis insensitive to naloxone. Our findings suggest a potential role for amygdalar arginine vasopressin in the aversive consequences of early cocaine withdrawal.

Amygdala↗
PubMed2005

Copeptin, a stable peptide derived from the vasopressin precursor, is elevated in serum of sepsis patients.

Vasopressin is one of the key regulators of the body's water and solute balance. When this balance is pathologically disturbed, determination of serum vasopressin concentrations might be a helpful tool for guiding therapy. However, due to its instability and considerable association to platelets, reliable measurement of circulating vasopressin is difficult to achieve, if at all. In search of a more robust way for quantifying vasopressin release, we identified copeptin, a glycopeptide with unknown function, as an alternative diagnostic target. Since copeptin is derived from the same precursor peptide as vasopressin, released amounts of copeptin should mirror those of vasopressin. With a newly developed sensitive sandwich immunoassay, we detected strongly elevated concentrations of fully processed copeptin in serum of septic shock patients. The magnitude of elevation and the high stability of copeptin in serum and plasma indicate that copeptin measurement is not affected by the problems, which are associated with the direct measurement of vasopressin, and thus is apparently suitable to indirectly determine the release of vasopressin.

Enzyme-Linked Immunosorbent Assay↗
PubMed2004

Peripheral vasopressin accelerates extinction of conditioned taste avoidance.

Both peripheral and central administration of vasopressin improves retention and delays extinction when given before or after acquisition of shock avoidance learning. For conditioned taste avoidance, however, vasopressin prolongs extinction when injected peripherally before acquisition tests and accelerates extinction when infused intracerebroventricularly after acquisition. The following experiments were designed to determine whether this inconsistency is based on the route of administration or timing of vasopressin treatment. Because acquisition of conditioned taste avoidance is strengthened when an agent that is capable of inducing avoidance is administered after LiCl injection, it was determined in experiment 1 that a 6 microg/kg dose of vasopressin did not induce conditioned taste avoidance when administered 50 min after consumption of a sucrose solution. In experiment 2, it was determined that this dose of vasopressin accelerated extinction of a LiCl-induced conditioned taste avoidance when given 50 min after LiCl injection. These results suggest that the inconsistency is not based on route of administration. In experiment 3, it was determined that there was a tendency for animals to show prolonged extinction when vasopressin was administered 20 min before access to a sucrose solution. All of the results taken together suggest that the differential effects of vasopressin on extinction are due to the timing of administration. It was suggested that vasopressin accelerates extinction when given after acquisition by reducing the effectiveness of LiCl and it prolongs extinction when given before acquisition by altering neural responsiveness in areas mediating conditioned taste avoidance.

Analysis of Variance↗
PubMed2005

High doses of vasopressin delay the onset of extinction and strengthen acquisition of LiCl-induced conditioned taste avoidance.

When low doses of vasopressin are given 50 min after pairing sucrose consumption with a high dose of LiCl, extinction of the LiCl-induced conditioned taste avoidance is accelerated. These low doses of vasopressin do not themselves induce conditioned taste avoidance when paired with sucrose consumption. Predicated on previous studies administering two avoidance-inducing agents after sucrose consumption, studies were designed to determine whether high doses of vasopressin capable of inducing conditioned taste avoidance would (1) delay rather than accelerate extinction of a conditioned taste avoidance induced by a high dose of LiCl and (2) strengthen acquisition of a conditioned taste avoidance induced by a low dose of LiCl. The results of three studies showed that doses of 9 and 18 microg/kg of vasopressin induced a conditioned taste avoidance when injected 50 min after sucrose consumption, delayed the onset of extinction when injected 50 min after pairing sucrose consumption with a high dose of LiCl, and strengthened acquisition of a conditioned taste avoidance when injected 50 min after pairing sucrose consumption with a low dose of LiCl. Taken together, these data suggest that the delay in onset of extinction is due to a strengthening of acquisition. It has been suggested that vasopressin is a mnemonic neuropeptide that delays extinction of learned tasks. However, for conditioned taste avoidance, the evidence for the effects of low doses of vasopressin on extinction do not support this hypothesis and the evidence for high doses of vasopressin can be accounted for by the avoidance-inducing properties of vasopressin.

Animals↗
PubMed2004

Effects of vasopressin on left anterior descending coronary artery blood flow during extremely low cardiac output.

UNLABELLED: Because of the possibility of vasopressin-mediated coronary vasospasm, this study was designed to assess effects of vasopressin compared to saline placebo on left anterior descending (LAD) coronary artery blood flow. Twelve anaesthetized domestic swine were prepared for LAD coronary artery blood flow measurement with ultrasonic flow probes, using cardiopulmonary by-pass adjusted to 10% of the prearrest cardiac output. This 10% value approximates that reported for cardiac output during conventional closed-chest CPR. After 4 min of untreated ventricular fibrillation, and 3 min of cardiopulmonary by-pass blood flow, 12 pigs were randomly assigned to receive intravenously, every 5 min, either vasopressin (0.4, 0.4, and 0.8 U/kg; n = 6) or saline placebo (n = 6). The mean +/- S.D. LAD coronary artery blood flow in the vasopressin and placebo pigs was comparable before cardiac arrest, and during cardiopulmonary by-pass low flow; but increased significantly (P < 0.05) 90 s after each of three vasopressin injections compared to placebo (78 +/- 1 versus 42 +/- 2 ml/min; 62 +/- 2 versus 36 +/- 1 ml/min; and 54 +/- 1 versus 27 +/- 1 ml/min), respectively. Coronary vascular resistance decreased significantly (P < 0.05 ) 90 s after each of three vasopressin and placebo injections. In this model, repeated bolus administration of vasopressin, given during simulated extremely low cardiac output improved LAD coronary artery blood flow to prearrest levels without affecting coronary vascular resistance. CONCLUSIONS: during extremely low blood flow using cardiopulmonary by-pass, vasopressin improves LAD coronary artery blood flow without affecting coronary vascular resistance.

Animals↗
PubMed2004

Vasopressin administered with epinephrine is associated with a return of a pulse in out-of-hospital cardiac arrest.

OBJECTIVE: Recent data suggest that using vasopressin in combination with epinephrine (adrenaline) may improve treatment of out-of-hospital cardiac arrest. This study examined local experience with the combination of epinephrine and vasopressin administration. METHODS: Data were obtained from an urban, municipal emergency medical service that does not include vasopressin in its formulary. A physician is dispatched to the scene of all cardiac arrest patients treated by this system. Vasopressin could be administered in addition to epinephrine to subjects with out-of-hospital cardiac arrest by the on-scene physician. Demographic information, drug administration and return of pulses were abstracted from patient care records for a 1-year interval. Multivariate logistic regression was used to assess the relationship between vasopressin use and outcomes. RESULTS: During the study period, data were available for 298 subjects receiving epinephrine-only (n=231, 78%), a combination of 40 IU vasopressin and epinephrine (n=37, 12%) or no vasopressor drugs (n=30, 10%). Among patients receiving vasopressor drugs, pulse was restored for 74 subjects (28%), and 56 subjects (21%) had a pulse on arrival at the hospital. Return of pulses was associated with witnessed collapse, bystander CPR, and an initial ECG rhythm of ventricular fibrillation or tachycardia. Subjects receiving vasopressin and epinephrine were more likely to have a return of pulses during the resuscitation (LR: 2.73; 95% CI: 1.24, 6.03) and at hospital arrival (3.85; 1.71, 8.65) than subjects treated with epinephrine alone. CONCLUSIONS: There is an association between using vasopressin in combination with epinephrine and restoration of circulation after out-of-hospital cardiac arrest.

Aged↗
PubMed1987

Vasopressin-induced bradycardia in fetal and adult sheep is not dependent on an increase in blood pressure.

Other investigators have reported that intravenous infusion of synthetic arginine vasopressin into fetal lambs increases mean arterial pressure and decreases heart rate. To determine if the bradycardia produced by arginine vasopressin is a reflex response to the increase in blood pressure, we studied the effect of arginine vasopressin infusion on heart rate with and without blocking the increase in blood pressure. We performed 34 experiments in 12 chronically cannulated fetal lambs between 103 and 137 days' gestation. All animals had normal blood gas and pH values. Infusion of arginine vasopressin increased mean arterial pressure 10.1 +/- 1.1 mm Hg and decreased heart rate 50 +/- 8 bpm. Fetal heart rate decreased similarly when arginine vasopressin was infused and the hypertensive response was blocked with nitroprusside or a selective vasoconstrictor antagonist. [1-(beta-mercapto-beta,beta-cyclopentamethylene propionic acid) 2-(O-methyl)tyrosine] arginine vasopressin. For comparison we also studied five adult nonpregnant ewes. Bradycardia was observed in the adults after infusion of arginine vasopressin alone and when the hypertensive response was blocked with the vasoconstrictor antagonist. We conclude that arginine vasopressin infusion causes a fall in heart rate independent of any increase in blood pressure in both the fetal lamb and the adult sheep.

Animals↗
PubMed2000

Vasopressin, major depression, and hypothalamic-pituitary-adrenocortical desensitization.

BACKGROUND: The hypothalamic neuropeptide arginine vasopressin is thought to play an important role in the pathophysiology of affective disorders and the hyperactivity of the hypothalamic-pituitary-adrenocortical system that frequently accompanies them. Postmortem studies as well as clinical investigations have described elevated levels of vasopressin in the brain and plasma of depressed patients, and this finding has been suggested to contribute to depressive symptomatology. METHODS: The case of a 47-year-old patient displaying chronically elevated plasma vasopressin levels due to paraneoplastic vasopressin secretion by an olfactory neuroblastoma and the first episode of major depression is presented. RESULTS: Depressive symptoms improved markedly after surgical resection of the tumor and subsequent normalization of plasma vasopressin levels. Unexpectedly, neither corticotropin nor cortisol secretion could be stimulated by an intravenous corticotropin-releasing hormone challenge under the condition of chronically elevated plasma vasopressin levels in this patient. CONCLUSIONS: Chronically elevated plasma vasopressin levels may induce depressive symptomatology, and-in contrast to the potent corticotropin secretagogue effects of acute vasopressin administration-lead to a marked desensitization of the hypothalamic-pituitary-adrenocortical system.

Adrenocorticotropic Hormone↗
PubMed2000

Vasopressin impairs K(ATP) and K(ca) channel function after brain injury.

This study was designed to characterize the role of vasopressin in impaired pial artery dilation to activators of the ATP sensitive K (K(ATP)) and calcium sensitive K (K(ca)) channel following fluid percussion brain injury (FPI) in newborn pigs equipped with a closed cranial window. Topical vasopressin was coadministered with the K(ATP) and K(ca) channel agonists cromakalim and NS1619 in a concentration approximating that observed in CSF following FPI. Vasopressin so administered attenuated pial artery dilation to these K(+) channel activators under conditions of equivalent baseline diameter during non injury conditions (13+/-1 and 23+/-1 vs. 4+/-1 and 10+/-2% for cromakalim 10(-8), 10(-6) M before and after vasopressin, respectively). Attenuated responses were fully restored when these agonists were coadministered with vasopressin and the vasopressin antagonist [l-(beta-mercapto-beta, beta-cyclopentamethylene propionic acid) 2-(o-methyl)-Tyr-AVP] (MEAVP). Cromakalim and NS1619 induced pial artery dilation was attenuated following FPI and MEAVP preadministration partially prevented such impairment (13+/-1 and 23+/-1, sham control; 2+/-1 and 5+/-1, FPI; and 9+/-1 and 15+/-2%, FPI-MEAVP pretreated for responses to cromakalim 10(-8), 10(-6) M, respectively). These data show that vasopressin blunts K(ATP) and K(ca) channel mediated cerebrovasodilation. These data suggest that vasopressin contributes to impaired K(ATP) and K(ca) channel function after brain injury.

Animals↗
PubMed2000

Neuromodulation of memory in the hippocampus by vasopressin.

The involvement of [Arg(8)]vasopressin in memory processes was analyzed in the hippocampal structure, since we have reported that this is one of the main central target structures of the vasopressin-enhancing effect on memory. This structure is functionally differentiated along its dorsoventral axis, and the expression of the vasopressinergic system is dependent upon whether the dorsal or ventral part of the hippocampus is involved. For this reason, the effect of vasopressin injected into hippocampus was evaluated on the basis of the site of injection. We have shown, using a Go-No Go visual discrimination task with mice that both parts of the hippocampus are involved in the effect of endogenous or exogenous vasopressin, but with higher sensitivity for the ventral part. Based on the expression of Fos protein following intracerebroventricular injection of vasopressin in unconditioned or conditioned mice, we confirmed the greater involvement of the ventral hippocampus in the enhancing effect of vasopressin on memory processes. The effect of the peptide seems specific, since only a few of the hippocampal cells that expressed Fos protein in the unconditioned mice did so in the conditioned mice (cells in the dentate gyrus and the CA3 hippocampal field). Moreover, we have shown that in the ventral hippocampus, vasopressin generates different behavioral effects whether treatment is performed at the beginning or in the middle of the learning process, suggesting that the mnemonic context is an important factor for understanding the effect of vasopressin on memory in the ventral hippocampus.

Animals↗
PubMed1988

Intravenous vasopressin and gastrointestinal hemorrhage in children.

Intravenous (IV) vasopressin has been used to control human upper gastrointestinal (GI) hemorrhage for over 30 years. Although the use of vasopressin has been studied extensively in adults, no study has evaluated its use in children. Vasopressin was used therapeutically in 15 episodes of esophageal variceal hemorrhage and two episodes of bleeding peptic ulcer. Nine of 17 episodes were controlled with vasopressin alone (53%). Balloon tamponade and variceal sclerosis were required for control in the remainder. Blood requirements averaged 53 mL/kg prior to control of hemorrhage. Metabolic complications occurred in 65% of the episodes. There were two groups of patients identified: those receiving greater or those receiving less than .01 units/kg/min of IV vasopressin. All of the complications identified occurred when greater than .01 U/kg/min of vasopressin were used (P less than .05). Control of bleeding was not improved with higher doses of vasopressin. These data suggest that the use of IV vasopressin at doses greater than .01 U/kg/min to control GI bleeding will increase the incidence of complications without improving control of hemorrhage.

Child↗