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Vasopressin
Kinds of Vasopressin Terms modified by Vasopressin Selected AbstractsPARTICIPATION OF VASOPRESSIN IN THE DEVELOPMENT OF CEREBRAL VASOSPASM IN A RAT MODEL OF SUBARACHNOID HAEMORRHAGECLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 4 2004Cristina C Trandafir SUMMARY 1.,Previous studies have suggested the involvement of arginine vasopressin (AVP) and inflammation in the development of cerebral vasospasm after subarachnoid haemorrhage (SAH). The aim of the present study was to clarify the role of AVP in the arterial narrowing following cerebral haemorrhage by examining the effect of SR 49059 (a V1 receptor antagonist) on the diameter of rat basilar artery exposed to SAH. The effect of the 5-lipoxygenase inhibitor ZM 230487 on AVP-induced contraction of rat basilar arteries was also investigated. 2.,After 1 h and 2 days from SAH induction, brains were removed and pictures of the basilar arteries were taken. The external diameter of the basilar artery was measured in the presence and absence of SR 49059 (1 mg/kg, i.v.). For in vitro experiments, the basilar arteries isolated from control and SAH rats (at 1 h and at 2 days from SAH induction) were cut into spiral preparations and the AVP (0.3 nmol/L)-induced contraction in the presence of ZM 230487 was investigated. Each group analysed (i.e. control, SAH 1 h and SAH 2 days) consisted of eight rats. 3.,The diameter of rat basilar arteries decreased by 43 and 25% at 1 h and 2 days from SAH induction, respectively, compared with control. The administration of SR 49059 significantly reduced cerebral vasospasm. After SAH induction, the diameter of the basilar artery in SR 49059-treated groups decreased by only 22% (at 1 h) and by 3% (at 2 days) compared with the control group (P < 0.01). In basilar arterial strips, ZM 230487 attenuated the vasopressin-induced contraction in both control and SAH groups. However, SAH groups showed a significant resistance of the AVP-induced contraction in the presence of ZM 230487 compared with control (P < 0.05). 4.,The results suggest that the cerebral vasospasm in SAH rats is due, at least in part, to endogenous AVP and may involve an increase in the activity of 5-lipoxygenase. SR 49059 may represent a potential therapeutic strategy for the treatment of cerebral vasospasm. [source] Losartan decreases vasopressin-mediated cAMP accumulation in the thick ascending limb of the loop of Henle in rats with congestive heart failureACTA PHYSIOLOGICA, Issue 4 2007M. Torp Abstract Introduction:, Vasopressin (AVP) stimulates sodium reabsorption and Na,K,2Cl-cotransporter (NKCC2) protein level in the thick ascending limb (TAL) of Henle's loop in rats. Rats with congestive heart failure (CHF) have increased protein level of NKCC2, which can be normalized by angiotensin II receptor type-1 (AT1) blockade with losartan. Aim:, In this study, we investigated whether CHF rats displayed changes in AVP stimulated cAMP formation in the TAL and examined the role of AT1 receptor blockade on this system. Method:, CHF was induced by ligation of the left anterior descending coronary artery (LAD). SHAM-operated rats were used as controls. Half of the rats were treated with losartan (10 mg kg day,1 i.p.). Results:, CHF rats were characterized by increased left ventricular end diastolic pressure. Measurement of cAMP in isolated outer medullary TAL showed that both basal and AVP (10,6 m) stimulated cAMP levels were significantly increased in CHF rats (25.52 ± 4.49 pmol cAMP ,g,1 protein, P < 0.05) compared to Sham rats (8.13 ± 1.14 pmol cAMP ,g,1 protein), P < 0.05). Losartan significantly reduced the basal level of cAMP in CHF rats (CHF: 12.56 ± 1.93 fmol ,g,1 protein vs. Los-CHF: 7.49 ± 1.08, P < 0.05), but not in Sham rats (SHAM: 4.66 ± 0.59 vs. Los-SHAM: 4.75 ± 0.71). AVP-mediated cAMP accumulation was absent in both groups treated with losartan (Los-SHAM: 4.75 ± 0.71 and Los-CHF: 7.49 ± 1.08). Conclusion:, The results indicate that the increased NKCC2 protein level in the mTAL from CHF rats is associated with increased cAMP accumulation in this segment. Furthermore, the finding that AT1 receptor blockade prevents AVP-mediated cAMP accumulation in both SHAM and CHF rats suggests an interaction between angiotensin II and AVP in regulation of mTAL Na reabsorption. [source] Role of oxytocin and vasopressin in the transitions of weaning in the ratDEVELOPMENTAL PSYCHOBIOLOGY, Issue 4 2004A. Kavushansky Abstract Sucklings (18-day-old) and weanlings (35-day-old) were injected icv with oxytocin or its antagonist (both 0.5 ,g/1 ,l), or vasopressin (1.0 ng/1 ,l) or its antagonist (100 ng/1 ,l), prior to 4-min observation in a behavioral maze with a sibling in one box and their anesthetized dam in the other. Oxytocin abolished nipple attachment in sucklings, decreased time spent with the dam, and increased self-grooming. The oxytocin antagonist had little influence on behavior. Vasopressin increased self-grooming while its antagonist reduced passive contact with the dam, increased active contact with her, and increased exploration and activity. We conclude that these neuropeptides have diverse roles during weaning, maintaining sucklings' behavior or promoting weaning, and subserving the transition from attachment to the dam to independence from her. We propose that these neurochemicals, and others, mediate the neural, affiliative, and affective changes of weaning, and that the term "weaning" should be understood to encompass these behavioral transitions. © 2004 Wiley Periodicals, Inc. Dev Psychobiol 45: 231,238, 2004. [source] Circulating levels of copeptin, a novel biomarker, in lower respiratory tract infectionsEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 2 2007B. Müller Abstract Background, Vasopressin has haemodynamic as well as osmoregulatory effects, and reflects the individual stress response. Copeptin is cosynthesized with vasopressin, directly mirroring vasopressin levels, but is more stable in plasma and serum. Both levels are increased in patients with septic shock. Lower respiratory tract infections (LRTI) are a precursor of sepsis. Thus, we investigated circulating levels and the prognostic use of copeptin for the severity and outcome in patients with LRTI. Materials and methods, Five hundred and forty-five consecutive patients with LRTI and 50 healthy controls were evaluated. Serum copeptin levels were measured with a new chemiluminescens sandwich immunoassay. Results, Of the 545 patients, 373 had community-acquired pneumonia (CAP), 60 acute exacerbations of chronic obstructive pulmonary disease (COPD), 59 acute bronchitis, 13 exacerbations of asthma and 40 other final diagnoses. Copeptin levels were significantly higher in patients with LRTI as compared to controls (P < 0·001) with highest levels in patients with CAP. Copeptin levels increased with increasing severity of CAP, as classified by the pneumonia severity index (PSI) (P < 0·001). In patients who died, copeptin levels on admission were significantly higher as compared to levels in survivors [70·0 (28·8,149·0) vs. 24·3 (10·8,43·8) pmol L,1, P < 0·001]. The area under the receiver operating curve (AUC) for survival was 0·75 for copeptin, which was significantly higher as compared to C-reactive protein (AUC 0·61, P = 0·01), leukocyte count (AUC 0·59, P = 0·01) and similar to procalcitonin (AUC 0·68, P = 0·21). Conclusions, Copeptin levels are increased with increasing severity of LRTI namely in patients with CAP and unfavourable outcome. Copeptin levels, as a novel biomarker, might be a useful tool in the risk stratification of patients with LRTI. [source] Vasopressin modulates lateral septal network activity via two distinct electrophysiological mechanismsEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 9 2007G. Allaman-Exertier Abstract The lateral septal area is rich in vasopressin V1A receptors and is densely innervated by vasopressinergic axons, originating mainly from the bed nucleus of the stria terminalis and the amygdala. Genetic and behavioral studies provide evidence that activation of vasopressin receptors in this area plays a determinant role in promoting social recognition. What could be the neuronal mechanism underlying this effect? Using rat brain slices and whole-cell recordings, we found that lateral septal neurons are under the influence of a basal GABAergic inhibitory input. Vasopressin, acting via V1A but not V1B receptors, greatly enhanced this input in nearly all neurons. The peptide had no effect on miniature inhibitory postsynaptic currents, indicating that it acted on receptors located in the somatodendritic membrane, rather than on axon terminals, of GABAergic interneurons. Cell-attached recordings showed that vasopressin can cause a direct excitation of a subpopulation of lateral septal neurons by acting via V1A but not V1B receptors. The presence in the lateral septum of V1A but not of V1B receptors was confirmed by competition binding studies using light microscopic autoradiography. In conclusion, vasopressin appears to act in the lateral septum in a dual mode: (i) by causing a direct excitation of a subpopulation of neurons, and (ii) by causing an indirect inhibition of virtually all lateral septal neurons. This modulation by vasopressin of the lateral septal circuitry may be part of the neuronal mechanism by which the peptide, acting via V1A receptors, promotes social recognition. [source] Renal Response to Arginine Vasopressin During the Oestrous Cycle in the Rat: Comparison of Glucose and Saline Infusion Using Physiological Doses of VasopressinEXPERIMENTAL PHYSIOLOGY, Issue 1 2002David E. Hartley The renal response to arginine vasopressin in the rat has been shown to depend on reproductive status. However there is no consensus as to when the kidney is most responsive. The varying results could depend on the protocol and the dose of hormone used. A study has been performed, with physiological doses of vasopressin, comparing the responses during infusion of hypotonic saline and glucose. After an equilibration period of 150 min, conscious rats were infused on each of the four days of the oestrous cycle with either isotonic saline (0.077 M) or 0.14 M glucose for a control period of 45 min. Vasopressin was then infused at 10-40 fmol min,1 for 1 h, followed by a recovery period of 90 min. Timed urine samples were collected for determination of volume, sodium concentration and osmolality. During the control period urine flow was greatest at oestrus and dioestrus day 2 and sodium excretion on dioestrus day 2 irrespective of the infusate. Vasopressin concentrations achieved lay within the physiological range and no difference was observed between the different days for a given dose. Infusion of vasopressin in both saline and glucose produced a dose-dependent antidiuresis, the greatest responses being seen of pro-oestrus and dioestrus day 2. It was only with the highest rate of infusion that a significant increase in sodium excretion was seen on each day of the cycle and the greatest responses were seen on pro-oestrus and dioestrus day 1 for both infusates. Thus the kidney shows the greatest response to physiological doses of vasopressin at pro-oestrus and dioestrus day 1 irrespective of the infusate employed. [source] The role of steroid hormones in the regulation of vasopressin and oxytocin release and mRNA expression in hypothalamo neurohypophysial explants from the ratEXPERIMENTAL PHYSIOLOGY, Issue 2000Celia D. Sladek Vasopressin and oxytocin release from the neural lobe, and the vasopressin and oxytocin mRNA contents of the supraoptic and paraventricular nuclei are increased by hypertonicity of the extracellular fluid. The factors regulating these parameters can be conveniently studied in perifused explants of the hypothalamo-neurohypophysial system that include the supraoptic nucleus (but not the paraventricular nucleus) with its axonal projections to the neural lobe. Vasopressin and oxytocin release and the mRNA content of these explants respond appropriately to increases in the osmolality of the perifusate. This requires synaptic input from the region of the organum vasculosum of the lamina terminalis. Glutamate is a likely candidate for transmitting osmotic information from the organum vasculosum of the lamina terminalis to the magnocellular neurones, because agonists for excitatory amino acid receptors stimulate vasopressin and oxytocin release, and because increased vasopressin release and mRNA content induced in hypothalamo-neurohypophysial explants by a ramp increase in osmolality are blocked by antagonists of both NMDA (N -methyl-D-aspartate) and non-NMDA glutamate receptors. Osmotically stimulated vasopressin release is also blocked by testosterone, dihydrotestosterone, oestradiol and corticosterone. Both oestrogen and dihydrotestosterone block NMDA stimulation of vasopressin release, and in preliminary studies oestradiol blocked AMPA stimulation of vasopressin release. Thus, steroid inhibition of osmotically stimulated vasopressin secretion may reflect inhibition of mechanisms mediated by excitatory amino acids. Recent studies have demonstrated numerous mechanisms by which steroid hormones may impact upon neuronal function. Therefore, additional work is warranted to understand these effects of the steroid hormones on vasopressin and oxytocin secretion and to elucidate the potential contribution of these mechanisms to regulation of hormone release in vivo. [source] Association of vasopressin 1a receptor levels with a regulatory microsatellite and behaviorGENES, BRAIN AND BEHAVIOR, Issue 5 2005E. A. D. Hammock Vasopressin regulates complex behaviors such as anxiety, parenting, social engagement and attachment and aggression in a species-specific manner. The capacity of vasopressin to modulate these behaviors is thought to depend on the species-specific distribution patterns of vasopressin 1a receptors (V1aRs) in the brain. There is considerable individual variation in the pattern of V1aR binding in the brains of the prairie vole species, Microtus ochrogaster. We hypothesize that this individual variability in V1aR expression levels is associated with individual variation in a polymorphic microsatellite in the 5, regulatory region of the prairie vole v1ar gene. Additionally, we hypothesize that individual variation in V1aR expression contributes to individual variation in vasopressin-dependent behaviors. To test these hypotheses, we first screened 20 adult male prairie voles for behavioral variation using tests that measure anxiety-related and social behaviors. We then assessed the brains of those animals for V1aR variability with receptor autoradiography and used polymerase chain reaction to genotype the same animals for the length of their 5, microsatellite polymorphism in the v1ar gene. In this report, we describe the results of this discovery-based experimental approach to identify potential gene, brain and behavior interrelationships. The analysis reveals that V1aR levels, in some but not all brain regions, are associated with microsatellite length and that V1aR levels in those and other brain regions correlate with anxiety-related and social behaviors. These results generate novel hypotheses regarding neural control of anxiety-related and social behaviors and yield insight into potential mechanisms by which non-coding gene polymorphisms may influence behavioral traits. [source] p.R254Q mutation in the aquaporin-2 water channel causing dominant nephrogenic diabetes insipidus is due to a lack of arginine vasopressin-induced phosphorylation,HUMAN MUTATION, Issue 10 2009Paul JM Savelkoul Abstract Vasopressin regulates human water homeostasis by re-distributing homotetrameric aquaporin-2 (AQP2) water channels from intracellular vesicles to the apical membrane of renal principal cells, a process in which phosphorylation of AQP2 at S256 by cAMP-dependent protein kinase A (PKA) is thought to be essential. Dominant nephrogenic diabetes insipidus (NDI), a disease in which the kidney is unable to concentrate urine in response to vasopressin, is caused by AQP2 gene mutations. Here, we investigated a reported patient case of dominant NDI caused by a novel p.R254Q mutation. Expressed in oocytes, AQP2-p.R254Q appeared to be a functional water channel, but was impaired in its transport to the cell surface to the same degree as AQP2-p.S256A, which mimics non-phosphorylated AQP2. In polarized MDCK cells, AQP2-p.R254Q was retained and was distributed similarly to that of unstimulated wt-AQP2 or AQP2-p.S256A. Upon co-expression, AQP2-p.R254Q interacted with, and retained wt-AQP2 in intracellular vesicles. In contrast to wild-type AQP2, forskolin did not increase AQP2-p.R254Q phosphorylation at S256 or its translocation to the apical membrane. Mimicking constitutive phosphorylation in AQP2-p.R254Q with the p.S256D mutation, however, rescued its apical membrane expression. These date indicate that a lack of S256 phosphorylation is the sole cause of dominant NDI here, and thereby, p.R254Q is a loss of function instead of a gain of function mutation in dominant NDI. © 2009 Wiley-Liss, Inc. [source] The Relationship Between the Action of Arginine Vasopressin and Responsiveness to Oral Desmopressin in Older Men: A Pilot StudyJOURNAL OF AMERICAN GERIATRICS SOCIETY, Issue 4 2007Theodore M. Johnson II OBJECTIVES: To identify whether oral desmopressin (ddAVP) reduced nocturnal urine volume (NUV) in older men with nocturia without obvious bladder outlet obstruction and to determine whether deficiencies in arginine vasopressin (AVP) release and action demonstrated using water deprivation testing predicted responsiveness to ddAVP. DESIGN: Participants had a 2-day Clinical Research Center (CRC) evaluation followed by a double-blinded, placebo-controlled, crossover trial of individually titrated oral ddAVP. SETTING: Participants were from a single Department of Veterans Affairs Medical Center. MEASUREMENTS: Maximum urine osmolality and percentage increase in osmolality were measured after subjects received aqueous vasopressin as part of the overnight water deprivation study; these data were used to categorize participants as normal, having partial central AVP deficiency, or having impaired renal responsiveness to AVP. Response to ddAVP was assessed using data from frequency-volume records. RESULTS: Fourteen participants completed the CRC stay and ddAVP trial. Subjects given ddAVP reduced NUV significantly from baseline (P=.02) and had significantly lower NUV than when on placebo (P=.01). The mean net reduction in NUV from ddAVP compared to placebo was 14±18%. Using water deprivation testing to categorize participants, 10 were normal, two had partial central AVP deficiency, and two had impaired renal responsiveness. The mean net reduction in NUV for those with abnormal water deprivation tests was 11±25%, versus 15±16% for those with normal water deprivation testing (P=.70). CONCLUSION: In this small randomized, controlled trial in older men with nocturia, ddAVP reduced NUV. Counter to expectations, participants deemed normal according to water deprivation tests had approximately equivalent responsiveness to ddAVP. Although this study cannot offer definitive conclusions on the lack of prediction of water deprivation testing for ddAVP benefit, these data offer additional information that may help clarify the pathophysiology and optimal treatment of nocturia in older men. [source] Low-dose vasopressin increases glomerular filtration rate, but impairs renal oxygenation in post-cardiac surgery patientsACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 8 2009G. BRAGADOTTIR Background: The beneficial effects of vasopressin on diuresis and creatinine clearance have been demonstrated when used as an additional/alternative therapy in catecholamine-dependent vasodilatory shock. A detailed analysis of the effects of vasopressin on renal perfusion, glomerular filtration, excretory function and oxygenation in man is, however, lacking. The objective of this pharmacodynamic study was to evaluate the effects of low to moderate doses of vasopressin on renal blood flow (RBF), glomerular filtration rate (GFR), renal oxygen consumption (RVO2) and renal oxygen extraction (RO2Ex) in post-cardiac surgery patients. Methods: Twelve patients were studied during sedation and mechanical ventilation after cardiac surgery. Vasopressin was sequentially infused at 1.2, 2.4 and 4.8 U/h. At each infusion rate, systemic haemodynamics were evaluated by a pulmonary artery catheter, and RBF and GFR were measured by the renal vein thermodilution technique and by renal extraction of 51chromium,ethylenediaminetetraacetic acid, respectively. RVO2 and RO2Ex were calculated by arterial and renal vein blood samples. Results: The mean arterial pressure was not affected by vasopressin while cardiac output and heart rate decreased. RBF decreased and GFR, filtration fraction, sodium reabsorption, RVO2, RO2Ex and renal vascular resistance increased dose-dependently with vasopressin. Vasopressin exerted direct antidiuretic and antinatriuretic effects. Conclusions: Short-term infusion of low to moderate, non-hypertensive doses of vasopressin induced a post-glomerular renal vasoconstriction with a decrease in RBF and an increase in GFR in post-cardiac surgery patients. This was accompanied by an increase in RVO2, as a consequence of the increases in the filtered tubular load of sodium. Finally, vasopressin impaired the renal oxygen demand/supply relationship. [source] Vasopressin decreases intestinal mucosal perfusion: a clinical study on cardiac surgery patients in vasodilatory shockACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 5 2009A. NYGREN Background: Low to moderate doses of vasopressin have been used in the treatment of cathecholamine-dependent vasodilatory shock in sepsis or after cardiac surgery. We evaluated the effects of vasopressin on jejunal mucosal perfusion, gastric-arterial pCO2 gradient and the global splanchnic oxygen demand/supply relationship in patients with vasodilatory shock after cardiac surgery. Methods: Eight mechanically ventilated patients, dependent on norepinephrine to maintain mean arterial pressure (MAP) ,60 mmHg because of septic/post-cardiotomy vasodilatory shock and multiple organ failure after cardiac surgery, were included. Vasopressin was sequentially infused at 1.2, 2.4 and 4.8 U/h for 30-min periods. Norepinephrine was simultaneously decreased to maintain MAP at 75 mmHg. At each infusion rate of vasopressin, data on systemic hemodynamics, jejunal mucosal perfusion, jejunal mucosal hematocrit and red blood cell velocity (laser Doppler flowmetry) as well as gastric-arterial pCO2 gradient (gastric tonometry) and splanchnic oxygen and lactate extraction (hepatic vein catheter) were obtained. Results: The cardiac index, stroke volume index and systemic oxygen delivery decreased and systemic vascular resistance and systemic oxygen extraction increased significantly, while the heart rate or global oxygen consumption did not change with increasing vasopressin dose. Jejunal mucosal perfusion decreased and the arterial-gastric-mucosal pCO2 gradient increased, while splanchnic oxygen or lactate extraction or mixed venous,hepatic venous oxygen saturation gradient were not affected by increasing infusion rates of vasopressin. Conclusions: Infusion of low to moderate doses of vasopressin in patients with norepinephrine-dependent vasodilatory shock after cardiac surgery induces an intestinal and gastric mucosal vasoconstriction. [source] Ageing and the Diurnal Expression of the mRNAs for Vasopressin and for the V1a and V1b Vasopressin Receptors in the Suprachiasmatic Nucleus of Male RatsJOURNAL OF NEUROENDOCRINOLOGY, Issue 6 2004T. Kalamatianos Abstract Changes in the function of neuropeptide synthesizing cells within the suprachiasmatic nucleus (SCN), the site of the predominant circadian pacemaker, may underlie the disturbance of rhythms observed during ageing. Arginine vasopressin (AVP) is synthesized by nearly one-third of SCN neurones in the rat. This peptide has predominantly excitatory actions within the SCN mediated by V1 -type receptors; the extent to which the V1a and/or V1b receptor subtypes are involved in SCN functions remains to be determined. The present study used isotopic in situ hybridization histochemistry to examine the effects of ageing on expression of mRNAs for AVP and V1a in the SCN and for V1b in the SCN and supraoptic nucleus (SON) of male rats kept under a 12 : 12 h light/dark cycle. Analysis of film autoradiographs from young adult (2,3-month-old; n = 40) or aged (19,20-month-old; n = 40) animals, at eight time points across the light/dark cycle, revealed an equivalent pattern and amplitude for the diurnal rhythm of AVP mRNA in the SCN of the young adult and aged groups. Both groups also displayed a significant diurnal rhythm in the expression of V1a receptor mRNA; however, the amplitude of this rhythm was reduced in the aged group, due to increased levels during the light phase and early part of night. Although the expression of V1b mRNA did not display a significant diurnal rhythm within the SCN or SON, persistently elevated levels for V1b mRNA were observed in the aged group at both sites. [source] In Vivo Gene Transfer Studies on the Regulation and Function of the Vasopressin and Oxytocin GenesJOURNAL OF NEUROENDOCRINOLOGY, Issue 2 2003D. Murphy Abstract Novel genes can be introduced into the germline of rats and mice by microinjecting fertilized one-cell eggs with fragments of cloned DNA. A gene sequence can thus be studied within the physiological integrity of the resulting transgenic animals, without any prior knowledge of its regulation and function. These technologies have been used to elucidate the mechanisms by which the expression of the two genes in the locus that codes for the neuropeptides vasopressin and oxytocin is confined to, and regulated physiologically within, specific groups of neurones in the hypothalamus. A number of groups have described transgenes, derived from racine, murine and bovine sources, in both rat and mouse hosts, that mimic the appropriate expression of the endogenous vasopressin and genes in magnocellular neurones (MCNs) of the supraoptic and paraventricular nuclei. However, despite considerable effort, a full description of the cis -acting sequences mediating the regulation of the vasopressin-oxytocin locus remains elusive. Two general conclusions have nonetheless been reached. First, that the proximal promoters of both genes are unable to confer any cell-specific regulatory controls. Second, that sequences downstream of the promoter, within the structural gene and/or the intergenic region that separates the two genes, are crucial for appropriate expression. Despite these limitations, sufficient knowledge has been garnered to specifically direct the expression of reporter genes to vasopressin and oxytocin MCNs. Further, it has been shown that reporter proteins can be directed to the regulated secretory pathway, from where they are subject to appropriate physiological release. The use of MCN expression vectors will thus enable the study of the physiology of these neurones through the targeted expression of biologically active molecules. However, the germline transgenic approach has a number of limitations involving the interpretation of phenotypes, as well as the large cost, labour and time demands. High-throughput somatic gene transfer techniques, principally involving the stereotaxic injection of hypothalamic neuronal groups with replication-deficient adenoviral vectors, are now being developed that obviate these difficulties, and which enable the robust, long-lasting expression of biologically active proteins in vasopressin and oxytocin MCNs. [source] Naturally Occurring Differences in Maternal Care are Associated with the Expression of Oxytocin and Vasopressin (V1a) Receptors: Gender DifferencesJOURNAL OF NEUROENDOCRINOLOGY, Issue 5 2002D. D. Francis Abstract Variations in maternal care have been associated with long-term changes in neurochemistry and behaviour in adult rats. Rats receiving high levels of licking and grooming as pups are less fearful and more maternal than rats receiving low levels of maternal licking and grooming. Central pathways for oxytocin and vasopressin have been implicated in the neurobiology of anxiety and social behaviours. We assessed whether variations in maternal care were associated with differences in oxytocin receptors (OTR) or vasopressin (V1a) receptors in the brains of adult offspring. In the central nucleus of the amygdala and bed nucleus of the stria terminalis, OTR binding was increased in adult females, but not adult males, that had received high levels of maternal licking and grooming as pups. Conversely, amygdala V1a receptor binding was increased in males, but not females, that had received high levels of maternal licking and grooming. These findings suggest that variations in maternal care may influence the expression of oxytocin and vasopressin receptors in a gender-specific manner. [source] Analysis of interactions responsible for vasopressin binding to human neurohypophyseal hormone receptors,molecular dynamics study of the activated receptor,vasopressin,G, systemsJOURNAL OF PEPTIDE SCIENCE, Issue 3 2006Magdalena J., lusarz Abstract Vasopressin (CYFQNCPRG-NH2, AVP) is a semicyclic endogenous peptide, which exerts a variety of biological effects in mammals. The main physiological roles of AVP are the regulation of water balance and the control of blood pressure and adrenocorticotropin hormone (ACTH) secretion, mediated via three different subtypes of vasopressin receptors: V1a, V1b and V2 receptors (V1aR, V1bR and V2R, respectively). They are the members of the class A, G-protein-coupled receptors (GPCRs). AVP also modulates several behavioral and social functions. In this study, the interactions responsible for AVP binding to vasopressin V1a and V2 receptors versus the closely related oxytocin ([I3,L8]AVP, OT) receptor (OTR) have been investigated. Three-dimensional models of the activated receptors were constructed using multiple sequence alignment, followed by homology modeling using the complex of activated rhodopsin with Gt,C -terminal peptide of transducin MII-Gt(338-350) prototype as a template. AVP was docked into the receptor-G, systems. The three lowest-energy pairs of receptor-AVP-G, (two complexes per each receptor) were selected. The 1-ns unconstrained molecular dynamics (MD) of complexes embedded into the fully hydrated 1-palmitoyl-2-oleoyl- sn -glycero-3-phosphatidylcholine (POPC) lipid bilayer was conducted in the AMBER 7.0 force field. Six relaxed receptor-AVP-G, models were obtained. The residues responsible for AVP binding to vasopressin receptors have been identified and a different mechanism of AVP binding to V2R than to V1aR has been proposed. Copyright © 2005 European Peptide Society and John Wiley & Sons, Ltd. [source] The use of vasopressin for treating vasodilatory shock and cardiopulmonary arrestJOURNAL OF VETERINARY EMERGENCY AND CRITICAL CARE, Issue 2 2009DACVIM, Richard D. Scroggin Jr. Abstract Objective , To discuss 3 potential mechanisms for loss of peripheral vasomotor tone during vasodilatory shock; review vasopressin physiology; review the available animal experimental and human clinical studies of vasopressin in vasodilatory shock and cardiopulmonary arrest; and make recommendations based on review of the data for the use of vasopressin in vasodilatory shock and cardiopulmonary arrest. Data Sources , Human clinical studies, veterinary experimental studies, forum proceedings, book chapters, and American Heart Association guidelines. Human and Veterinary Data Synthesis , Septic shock is the most common form of vasodilatory shock. The exogenous administration of vasopressin in animal models of fluid-resuscitated septic and hemorrhagic shock significantly increases mean arterial pressure and improves survival. The effect of vasopressin on return to spontaneous circulation, initial cardiac rhythm, and survival compared with epinephrine is mixed. Improved survival in human patients with ventricular fibrillation, pulseless ventricular tachycardia, and nonspecific cardiopulmonary arrest has been observed in 4 small studies of vasopressin versus epinephrine. Three large studies, though, did not find a significant difference between vasopressin and epinephrine in patients with cardiopulmonary arrest regardless of initial cardiac rhythm. No veterinary clinical trials have been performed using vasopressin in cardiopulmonary arrest. Conclusion , Vasopressin (0.01,0.04 U/min, IV) should be considered in small animal veterinary patients with vasodilatory shock that is unresponsive to fluid resuscitation and catecholamine (dobutamine, dopamine, and norepinephrine) administration. Vasopressin (0.2,0.8 U/kg, IV once) administration during cardiopulmonary resuscitation in small animal veterinary patients with pulseless electrical activity or ventricular asystole may be beneficial for myocardial and cerebral blood flow. [source] Vasopressin in paediatric practicePEDIATRIC ANESTHESIA, Issue 7 2008ANDREW WOLF No abstract is available for this article. [source] Vasopressin in the treatment of vasodilatory shock in childrenPEDIATRICS INTERNATIONAL, Issue 2 2005Satoshi Masutani Abstract,Background:,Many recent studies suggest that vasopressin deficiency is an important cause of catecholamine-resistant hypotension with vasodilation in adults, but little is known about vasopressin deficiency in children. Methods:,To clarify the usefulness of vasopressin administration in pediatric cathecolamine-resistant hypotension with preserved ventricular contractility, urinary output and blood pressure response to vasopressin were retrospectively analyzed in 12 consecutive patients (15 instances) who were treated with vasopressin. The causes of vasodilation were central nervous system disturbance (n = 5), side-effect of drug (n = 5), and infection (n = 5). Plasma vasopressin concentration was measured six times before vasopressin administration and five times during vasopressin administration. Results:,Patients were divided into four groups according to their response to vasopressin administration. In group 1 (n = 5), urinary output increased to > 3 mL/kg per h within 3 h after vasopressin administration. In group 2 (n = 4), urinary output increased to > 3 mL/kg per h from 3 to 5 h after vasopressin administration. In group 3 (n = 4), urinary output did not increase to > 3 mL/kg per min within 5 h after vasopressin administration, but systolic blood pressure increased to > 120% of the level at the time of vasopressin administration. All remaining patients were classified into group 4 (n = 3). Plasma vasopressin concentration were low considering the markedly hypotensive state in all six instances. Plasma vasopressin concentration during vasopressin administration were significantly increased compared with before administration (P < 0.05). No apparent side-effects were observed in this series. Conclusion:,Vasopressin deficiency may occur in catecholamine-resistant hypotension of pediatric patients due to various causes including central nervous system disturbance, drug induced hypotension and sepsis. Small doses of vasopressin administration seems to be very effective in such conditions by increasing blood pressure and urinary output. [source] Copeptin: A novel, independent prognostic marker in patients with ischemic stroke,ANNALS OF NEUROLOGY, Issue 6 2009Mira Katan MD Objective Early prediction of outcome in patients with ischemic stroke is important. Vasopressin is a stress hormone. Its production rate is mirrored in circulating levels of copeptin, a fragment of provasopressin. We evaluated the prognostic value of copeptin in acute stroke patients. Methods In a prospective observational study, copeptin was measured using a new sandwich immunoassay on admission in plasma of 362 consecutive patients with an acute ischemic stroke. The prognostic value of copeptin to predict the functional outcome (defined as a modified Rankin Scale score of ,2 or ,3), mortality within 90 days, was compared with the National Institutes of Health Stroke Scale score and with other known outcome predictors. Results Patients with an unfavorable outcomes and nonsurvivors had significantly increased copeptin levels on admission (p <0.0001 and p <0.0001). Receiver operating characteristics to predict functional outcome and mortality demonstrated areas under the curve of copeptin of 0.73 (95% confidence interval [CI], 0.67,0.78) and 0.82 (95% CI, 0.76,0.89), which was comparable with the National Institutes of Health Stroke Scale score but superior to C-reactive protein and glucose (p <0.01). In multivariate logistic regression analysis, copeptin was an independent predictor of functional outcome and mortality, and improved the prognostic accuracy of the National Institutes of Health Stroke Scale to predict functional outcome (combined areas under the curve, 0.79; 95% CI, 0.74,0.84; p <0.01) and mortality (combined areas under the curve, 0.89; 95% CI, 0.84,0.94; p <0.01). Interpretation Copeptin is a novel, independent prognostic marker improving currently used risk stratification of stroke patients. Ann Neurol 2009;66:799,808 [source] Effects of desmopressin on the sleep of children suffering from enuresisACTA PAEDIATRICA, Issue 7 2010C Rahm Abstract Aim:, To evaluate the effect of 1-desamino-8-D-Arginine Vasopressin (DDAVP) on sleep architecture and arousal reactions in children with primary monosymptomatic nocturnal enuresis (PME). Methods:, A prospective, placebo-controlled, randomized, double-blind, cross-over study was performed on children suffering from bed-wetting. Placebo and DDAVP were given for 7 days each after which an unattended home polysomnography (PSG) was recorded. After lifting the blinding, the PSGs were compared. Results:, A total of 20 children with PME, aged 6,15 years, were enrolled in the study. The number of wet nights decreased significantly with DDAVP treatment. Delta power, distribution of sleep stages, number of arousals, arousal index and the effect of arousals on sleep stages did not differ significantly. Bed-wetting occurred within each sleep stage and did not follow any particular pattern. In most cases, it was preceded by an arousal reaction, but no awakening occurred. Conclusion:, DDAVP has no effect on the sleep architecture of children with PME when analysed by classical PSG, which is determined by collecting the electric activity of cortical neurons. Taking recent research findings into account, this supports the thesis that the disturbances causing PME occur at brain stem level and do not reach consciousness. [source] Vasopressin in catecholamine-resistant septic and cardiogenic shock in very-low-birthweight infantsACTA PAEDIATRICA, Issue 10 2006Sascha Meyer Abstract Aim: To evaluate vasopressin as a rescue therapy in catecholamine-refractory septic and cardiogenic shock in very-low-birthweight (VLBW) infants. Methods: Prospective assessment of vasopressin therapy in three VLBW infants with catecholamine-refractory septic shock (24+.6 wk, 600 g) and cardiogenic shock (26+.1 wk, 890 g; 26+.1 wk, 880 g) at a university hospital. Results: Adequate systemic arterial blood pressure could only be restored after vasopressin administration as a continuous infusion over a 36-h period in the preterm suffering from septic shock; in the two neonates with cardiogenic shock, only a transient stabilization in mean arterial pressure was observed, which did not impact on the poor prognosis. Conclusion: Although vasopressin appears to be a suitable rescue therapy in catecholamine-resistant septic shock in VLBW infants, further evaluation in controlled clinical trials is warranted. [source] Area Postrema And Sympathetic Nervous System Effects Of Vasopressin And Angiotensin IICLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 5-6 2000Eileen M Hasser SUMMARY 1. Precise control over the cardiovascular system requires the integration of both neural and humoral signals related to blood volume and blood pressure. Humoral signals interact with neural systems, modulating their control over the efferent mechanisms that ultimately determine the level of pressure and volume. 2. Peptide hormones such as angiotensin (Ang)II and arginine vasopressin (AVP) act through circumventricular organs (CVO) to influence cardiovascular regulation. 3. The area postrema (AP), a CVO in the brainstem, mediates at least some of the central actions of these peptides. Vasopressin appears to act in the AP to cause sympathoinhibition and a shift in baroreflex control of the sympathetic nervous system (SNS) to lower pressures. These effects of AVP and the AP appear to be mediated by ,2 -adrenoceptor and glutamatergic mechanisms in the nucleus tractus solitarius. 4. In contrast to AVP AngII has effects in the AP to blunt baroreflex control of heart rate and cause sympathoexcitation. The effects of chronic AngII to increase activity of the SNS may be due to AP-dependent activation of neurons in the rostral ventrolateral medulla. [source] Copeptin: A Biomarker of Cardiovascular and Renal FunctionCONGESTIVE HEART FAILURE, Issue 2010Nils G. Morgenthaler MD Congest Heart Fail. 2010;16(4)(suppl 1):S37,S44. ©2010 Wiley Periodicals, Inc. Arginine vasopressin (AVP or antidiuretic hormone) is one of the key hormones in the human body responsible for a variety of cardiovascular and renal functions. It has so far escaped introduction into the routine clinical laboratory due to technical difficulties and preanalytical errors. Copeptin, the C-terminal part of the AVP precursor peptide, was found to be a stable and sensitive surrogate marker for AVP release. Copeptin behaves in a similar manner to mature AVP in the circulation, with respect to osmotic stimuli and hypotension. During the past years, copeptin measurement has been shown to be of interest in a variety of clinical indications, including cardiovascular diseases such as heart failure, myocardial infarction, and stroke. This review summarizes the recent progress on the diagnostic use of copeptin in cardiovascular and renal diseases and discusses the potential use of copeptin measurement in the context of therapeutic interventions with vasopressin receptor antagonists. [source] Hyponatremia and Heart Failure,Treatment ConsiderationsCONGESTIVE HEART FAILURE, Issue 1 2006Domenic A. Sica MD Hyponatremia as it occurs in the heart failure patient is a multifactorial process. The presence of hyponatremia in the heart failure patient correlates with both the severity of the disease and its ultimate outcome. The therapeutic approach to the treatment of hyponatremia in heart failure has traditionally relied on attempts to improve cardiac function while at the same time limiting fluid intake. In more select circumstances, hypertonic saline, loop diuretics, and/or lithium or demeclocycline have been used. The latter two compounds act by retarding the antidiuretic effect of vasopressin but carry with their use the risk of serious renal and/or cardiovascular side effects. Alternatively, agents that selectively block the type 2 vasopressin receptor increase free water excretion without any of the adverse consequences of other therapies. Conivaptan, lixivaptan, and tolvaptan are three such aquaretic drugs. Vasopressin receptor antagonists will redefine the treatment of heart failure-related hyponatremia and may possibly evolve as adjunct therapies to loop diuretics in diuretic-resistant patients. [source] Effect of angiotensin II and endothelin-1 receptor blockade on the haemodynamic and hormonal changes after acute blood loss and after retransfusion in conscious dogsACTA PHYSIOLOGICA, Issue 4 2004R. C. E. Francis Abstract Aim:, This study investigates angiotensin II and endothelin-1 mediated mechanisms involved in the haemodynamic, hormonal, and renal response towards acute hypotensive haemorrhage. Methods:, Conscious dogs were pre-treated with angiotensin II type 1 (AT1) and/or endothelin-A (ETA) receptor blockers or not. Protocol 1: After a 60-min baseline period, 25% of the dog's blood was rapidly withdrawn. The blood was retransfused 60 min later and data recorded for another hour. Protocol 2: Likewise, but preceded by AT1 blockade with i.v. Losartan. Protocol 3: Likewise, but preceded by ETA blockade with i.v. ABT-627. Protocol 4: Likewise, but with combined AT1plus ETAblockade. Results:, In controls, haemorrhage decreased mean arterial pressure (MAP) by approximately 25%, cardiac output by approximately 40%, and urine volume by approximately 60%, increased angiotensin II (3.1-fold), endothelin-1 (1.13-fold), vasopressin (116-fold), and adrenaline concentrations (3.2-fold). Glomerular filtration rate and noradrenaline concentrations remained unchanged. During AT1 blockade, the MAP decrease was exaggerated (,40%) and glomerular filtration rate fell. During ETA blockade, noradrenaline increased after haemorrhage instead of adrenaline, and the MAP recovery after retransfusion was blunted. The decrease in cardiac output was similar in all protocols. Conclusions:, Angiotensin II is more important than endothelin-1 for the short-term regulation of MAP and glomerular filtration rate after haemorrhage, whereas endothelin-1 seems necessary for complete MAP recovery after retransfusion. After haemorrhage, endothelin-1 seems to facilitate adrenaline release and to blunt noradrenaline release. Haemorrhage-induced compensatory mechanisms maintain blood flow more effectively than blood pressure, as the decrease in cardiac output , but not MAP , was similar in all protocols. [source] Influence of neurohumoral blockade on heart rate and blood pressure responses to haemorrhage in isoflurane anaesthetized ratsACTA PHYSIOLOGICA, Issue 3 2000UllmanArticle first published online: 24 DEC 200 Four groups of Sprague,Dawley rats were anaesthetized with isoflurane (ISO) (1.7% end-tidal concentration) in 40% oxygen, and mechanically ventilated. The animals were bled 15 mL kg,1 b.w. from the femoral vein over 10 min, followed by an observation period of 30 min. Ten minutes before haemorrhage each group of animals was pre-treated with intravenous injection/infusion of either: isotonic saline (Group B; CON; n=7), vasopressin V1 -receptor antagonist [d(CH2)5Tyr(Me)AVP; 10 ,g kg,1] (Group C; AVP-a; n=7), the non-selective angiotensin II receptor antagonist saralasin (10 ,g kg,1 min,1) (Group D; SAR; n=7) or hexamethonium (10 mg kg,1) (Group E; HEX; n=7). A separate group of conscious animals were pre-treated with isotonic NaCl and subjected to the same haemorrhage protocol (Group A; AW; n=7). Mean arterial pressure (MAP), heart rate (HR) and blood gases were observed during the experiments. Only pre-treatment with SAR and HEX reduced MAP significantly. The pre-haemorrhage HR was only affected by HEX, which caused a reduction by 17%. The HR was significantly lower at the end of haemorrhage compared with pre-haemorrhage levels in all groups except that group treated with HEX. In that group the HR changed in the opposite direction. The ability to maintain MAP during haemorrhage, and the post-haemorrhage period, was significantly impaired in the groups treated with AVP-a, SAR or HEX compared with the group receiving NaCl. It is concluded that autonomic nervous activity is of major importance for the maintenance of MAP during isoflurane anaesthesia, whereas circulating angiotensin II and vasopressin levels contribute to a much smaller degree in this regard. General anaesthesia in combination with different degrees of neurohumoral blockade impairs the haemodynamic responses to blood loss, seen in conscious individuals. The impairment involves both the early and late phases during haemorrhage, as well as the post-bleeding recovery period. All three neurohumoral systems (autonomic nervous activity, angiotensin II and vasopressin) are of importance for regulating MAP during and after haemorrhage, although the autonomic nervous outflow appears to contribute to a larger extent. [source] Forearm vascular and neuroendocrine responses to graded water immersion in humansACTA PHYSIOLOGICA, Issue 2 2000Gabrielsen The hypothesis that graded expansion of central blood volume by water immersion to the xiphoid process and neck would elicit a graded decrease in forearm vascular resistance was tested. Central venous pressure increased (P < 0.05) by 4.2 ± 0.4 mmHg (mean ± SEM) during xiphoid immersion and by 10.4 ± 0.5 mmHg during neck immersion. Plasma noradrenaline was gradually suppressed (P < 0.05) by 62 ± 8 and 104 ± 11 pg mL,1 during xiphoid and neck immersion, respectively, indicating a graded suppression of sympathetic nervous activity. Plasma concentrations of arginine vasopressin were suppressed by 1.5 ± 0.5 pg mL,1 (P < 0.05) during xiphoid immersion and by 2.0 ± 0.5 pg mL,1 during neck immersion (P < 0.05 vs. xiphoid immersion). Forearm subcutaneous vascular resistance decreased to the same extent by 26 ± 9 and 28 ± 4% (P < 0.05), respectively, during both immersion procedures, whereas forearm skeletal muscle vascular resistance declined only during neck immersion by 27 ± 6% (P < 0.05). In conclusion, graded central blood volume expansion initiated a graded decrease in sympathetic nervous activity and AVP-release. Changes in forearm subcutaneous vascular resistance, however, were not related to the gradual withdrawal of the sympathetic and neuroendocrine vasoconstrictor activity. Forearm skeletal muscle vasodilatation exhibited a more graded response with a detectable decrease only during immersion to the neck. Therefore, the forearm subcutaneous vasodilator response reaches saturation at a lower degree of central volume expansion than that of forearm skeletal muscle. [source] Ontogeny of vasotocin-expressing cells in zebrafish: Selective requirement for the transcriptional regulators orthopedia and single-minded 1 in the preoptic areaDEVELOPMENTAL DYNAMICS, Issue 4 2008Jennifer L. Eaton Abstract The neurohypophysial peptide arginine vasotocin, and its mammalian ortholog arginine vasopressin, influence a wide range of physiological and behavioral responses, including aspects of sexual and social behaviors, osmoregulation, stress response, metabolism, blood pressure, and circadian rhythms. Here, we demonstrate that, in zebrafish (Danio rerio), the vasotocin precursor gene arginine vasotocin-neurophysin (avt) is expressed in two domains in the developing embryo: the dorsal preoptic area and the ventral hypothalamus. In the dorsal preoptic area, avt -expressing cells are intermingled with isotocin-neurophysin (ist) -expressing cells, and these neurons project to the neurohypophysis (posterior pituitary). In the dorsal preoptic area, the transcriptional regulators orthopedia b (otpb) and simple-minded 1 (sim1) are required for expression of both avt and ist. In contrast, otp and sim1 are not required for avt expression in the ventral hypothalamus. Thus, the development of these two avt expression domains is influenced by separate gene regulatory networks. Developmental Dynamics 237:995,1005, 2008. © 2008 Wiley-Liss, Inc. [source] The zebrafish bHLH PAS transcriptional regulator, single-minded 1 (sim1), is required for isotocin cell developmentDEVELOPMENTAL DYNAMICS, Issue 8 2006Jennifer L. Eaton Abstract A wide range of physiological and behavioral processes, such as social, sexual, and maternal behaviors, learning and memory, and osmotic homeostasis are influenced by the neurohypophysial peptides oxytocin and vasopressin. Disruptions of these hormone systems have been linked to several neurobehavioral disorders, including autism, Prader-Willi syndrome, affective disorders, and obsessive-compulsive disorder. Studies in zebrafish promise to reveal the complex network of regulatory genes and signaling pathways that direct the development of oxytocin- and vasopressin-like neurons, and provide insight into factors involved in brain disorders associated with disruption of these systems. Isotocin, which is homologous to oxytocin, is expressed early, in a simple pattern in the developing zebrafish brain. Single-minded 1 (sim1), a member of the bHLH-PAS family of transcriptional regulatory genes, is required for terminal differentiation of mammalian oxytocin cells and is a master regulator of neurogenesis in Drosophila. Here we show that sim1 is expressed in the zebrafish forebrain and is required for isotocin cell development. The expression pattern of sim1 mRNA in the embryonic forebrain is dynamic and complex, and overlaps with isotocin expression in the preoptic area. We provide evidence that the role of sim1 in zebrafish neuroendocrine cell development is evolutionarily conserved with that of mammals. Developmental Dynamics 235:2071,2082, 2006. © 2006 Wiley-Liss, Inc. [source] | |||||||||||||||||||||||||||||||||||||