Plasma Vasopressin Levels Research Articles

Urinary aquaporin-2 is elevated in infant atopic dermatitis

Conflicts of interest: none declared. Madam, One of the key features of atopic dermatitis (AD) is increased transepidermal water loss (TEWL),1, 2 a phenomenon attributable partly to impaired barrier function of the skin due to some genetic defects such as filaggrin gene (FLG) mutations, or to inflammatory status in AD.1 Remarkable loss of body fluid would induce a series of systemic regulatory reactions. The functional antidiuretic hormone (ADH)–aquaporin (AQP)‐2 axis is a major regulatory system to keep water balance. AQP‐2 mediates water transport across the apical plasma membrane of the renal collecting ducts. Kidney AQP‐2 expression can be estimated quantitatively by urinary excretion of AQP‐2. Moreover, the amount of urinary AQP‐2 (u‐AQP‐2) is positively correlated with the plasma levels of ADH in normal subjects.3 Increased serum ADH was detected in severe AD, a result possibly due to a dehydrated state caused by increased TEWL in these patients.2 Therefore, it is possible that u‐AQP‐2 is altered in AD. We conducted a case–control study to measure the u‐AQP‐2 level in paediatric patients with AD, and assessed its correlation with several clinical and laboratory parameters.

Effect of estrogens on plasma vasopressin and renin activity in postmenopausal women.

The effects of estrogens on plasma vasopressin and renin activity were investigated in 18 postmenopausal women. After an oral estrogen therapy (1 mg estradiol valerate + 2mg estriol succinate/day) of three weeks duration the plasma vasopressin level was decreased (p<0.05). The basic levels of vasopressin and PRA and those after one, three and 24 hours after an intramuscular injection of 10 mg estradiol valerate did not differ significantly.

Autoimmunity to the Sodium-Level Sensor in the Brain Causes Essential Hypernatremia

Na(x) is the sodium-level sensor of body fluids in the brain involved in sodium homeostasis. Na(x)-knockout mice do not stop ingesting salt even when dehydrated. Here we report a case with clinical features of essential hypernatremia without demonstrable hypothalamic structural lesions, who was diagnosed as a paraneoplastic neurologic disorder. The patient had autoantibodies directed against Na(x), along with a ganglioneuroma composed of Schwann-like cells robustly expressing Na(x). The removal of the tumor did not reduce the autoantibody levels or relieve the symptoms. Intravenous injection of the immunoglobulin fraction of the patient's serum into mice induced abnormalities in water/salt intake and diuresis, which led to hypernatremia. In the brains of these mice, cell death was observed along with focal deposits of complement C3 and inflammatory infiltrates in circumventricular organs where Na(x) is specifically expressed. Our findings thus provide new insights into the pathogenesis of hypernatremia relevant to the sodium-level-sensing mechanism in humans.

Effect of repeatedly given CDP-choline on cardiovascular and tissue injury in spinal shock conditions: investigation of the acute phase

The protective effect of CDP-choline in spinal cord transection and the mediation of its cardiovascular effects were investigated. Spinal cords of rats were transected at the T1-T2 levels. CDP-choline (250 mg/kg; intravenous) was administered 2 h and/or 24 h after the injury. Spinal cord transection caused severe tissue damage, decreased mean arterial pressure, heart rate, plasma adrenaline, and noradrenaline but increased plasma vasopressin levels. Repeated CDP-choline treatment attenuated the degree of tissue injury. Administration of CDP-choline at 2 h after transection transiently increased blood pressure and decreased heart rate, while it produced a small decrease in blood pressure and heart rate when it was given at 24 h. Plasma adrenaline levels were higher in the group where CDP-choline was given repeatedly. Plasma noradrenaline and vasopressin levels did not change additionally after CDP-choline injections in all groups. In order to determine if CDP-choline attenuates the oxidative injury induced by transection, we measured blood superoxide dismutase, glutathione peroxidase activity and malondialdehyde levels. Repeated CDP-choline administration decreased blood superoxide dismutase and glutathione peroxidase activity without any effect on malondialdehyde levels. Data indicate that repeated intravenous CDP-choline treatment prevents tissue damage in spinal shock conditions in the acute phase. The cardiovascular effects of the drug do not seem to be responsible for this protection but the drug-induced attenuation of the oxidative stress may play a role.

The blockade of oxytocinergic receptors in the CeA modify VP plasma levels and mRNA expression induced by hypertonic BVE in the rat.

We investigated the effects of oxytocin (OT) and the oxytocinergic antagonist vasotocin (OVT) injection in the central amygdala (CeA) in the regulation of vasopressin (VP) mRNA expression in the hypothalamus and VP plasma levels in response to hypertonic blood volume expansion (hyper BVE). Male Wistar rats with cannulas unilaterally in the CeA were subjected to BVE (2 ml/100 g bw) over 1 minute. OT, OVT or vehicle was injected into the CeA 20 min before the BVE. Five min after BVE rats were decapitated and the blood was collected for VP plasma determination. Another group was perfused 40 min after BVE. Brain sections of the paraventricular (Pa) and the supraoptic (SON) nuclei were collected for in situ hybridization using a 35S‐labeled VP probe. OT injection in the CeA increased plasma VP levels after hyper BVE and reduced VP mRNA in the PaLM. OVT reduced plasma AVP levels following a reduction VP mRNA in the PaLM and SON. Our data suggest that OT in the CeA may modulate the physiological mechanisms involved in plasma AVP release but the time course of the hormonal release has been shown dissociated from the genomic AVP expression in the PaLM. We hypothesize that the blockade of OT CeA receptors with OVT may activate an inhibitory input to vasopressinergic magnocellular neurons in the hypothalamus leading to the decrease in plasma AVP levels that can be strongly correlated with the reduction in the genomic AVP mRNA.

Influences of hypertonic and hypovolemic treatments on vasopressin response in propylthiouracil (PTU) induced hypothyroid rat and effect on supplementation with L-thyroxine

This study was performed to investigate the effects of L-thyroxine treatment on plasma vasopressin (AVP) levels in rats with hypothyroidism induced by propylthiouracil (PTU). Animals were separated into three groups each having 6 rats: control, PTU, PTU+L-thyroxine groups. Then, the groups were further divided into 3 sub-groups including 6 rats (a; basal, b; hypertonic stimulated and c; hypovolemic stimulated). At the end of the experiments all rats were decapitated in order to obtain plasma samples for analysis in terms of Hct, osmolality, TT 3 , TT 4 and vasopressin. Haematocrit (Hct) levels were the highest in hypovolemic stimulated sub-group (P < 0.001). Osmolality levels were higher in hypertonic stimulated sub-groups (P < 0.001). Total T 3 and T 4 values were the lowest in the PTU group and the highest in the L-thyroxine treated group (P < 0.001). Plasma AVP levels were reduced by hypothyroidism. However, L-thyroxine treatment after the hypothyroidism prevented this reduction (P < 0.001). Vasopressin responses to basal, hypovolemic and hypertonic stimulations were the lowest in the PTU group (P < 0.001). The results of the present study show that basal and stimulated plasma vasopressin levels are reduced in PTU-induced hypothyroidism. However, L-thyroxine treatment following hypothyroidism prevents this reduction.

Diagnostic Value of Plasma Antidiuretic Hormone, Electrocochleography, and Glycerol Test in Patients with Endolymphatic Hydrops

Objective: To investigate the relationship between the plasma antidiuretic hormone (p-ADH) level, electrocochleogram (ECoG), and the glycerol test in patients with endolymphatic hydrops (ELH). Patients and Methods: The subjects were 60 patients, including 51 with Ménière’s disease (except for cochlear Ménière’s disease), 7 with delayed ELH, and 2 with syphilitic ELH. The time period for measurements of the p-ADH level, ECoG and the glycerol test was within 4 weeks. Results: 13 patients showed positive results for all tests. 58 patients showed positive results for at least one of three tests. Only 2 patients showed negative results for all tests. Conclusion: The p-ADH level, ECoG and the glycerol test show different selectivity of ELH detection. It is useful to perform all three tests to diagnose ELH.

Central Adrenal Insufficiency and Diabetes Insipidus Misdiagnosed as Severe Depression

A 68 year-old Japanese man, who had been suffering from immobilization and disuse syndrome, was admitted to our hospital for evaluation of polyuria with polyposia, hyponatremia and low blood pressure. His plasma osmolality was greater than that of his urine. His endocrinological examination revealed low levels of plasma adrenocorticotropic hormone (ACTH) and cortisol, and a normal response of ACTH to the corticotrophin-releasing hormone (CRH) challenge. Plasma ACTH did not increase with insulin loading. A low plasma vasopressin (AVP) level and no response of AVP to a 5% saline administration were observed. We diagnosed central adrenal insufficiency with central diabetes insipidus. Six months after starting administration of hydrocortisone and 1-deamino-8D-arginine vasopressin, his psychological symptoms had improved, and 1.5 years after starting treatment, he was able to walk. In conclusion, it is not particularly rare for adrenal insufficiency to be misdiagnosed as depression. However, a correct early diagnosis is necessary, because, if adrenal insufficiency is not definitively diagnosed, the patient's quality of life diminishes markedly.

Central nitrergic system regulation of neuroendocrine secretion, fluid intake and blood pressure induced by angiotensin-II

BackgroundNitric oxide (NO) synthesis has been described in several circumventricular and hypothalamic structures in the central nervous system that are implicated in mediating central angiotensin-II (ANG-II) actions during water deprivation and hypovolemia. Neuroendocrine and cardiovascular responses, drinking behavior, and urinary excretions were examined following central angiotensinergic stimulation in awake freely-moving rats pretreated with intracerebroventricular injections of Nω-nitro-L-arginine methyl ester (L-NAME, 40 μg), an inhibitor of NO synthase, and L-arginine (20 ug), a precursor of NO.ResultsInjections of L-NAME or ANG-II produced an increase in plasma vasopressin (VP), oxytocin (OT) and atrial natriuretic peptide (ANP) levels, an increase in water and sodium intake, mean arterial blood pressure and sodium excretion, and a reduction of urinary volume. L-NAME pretreatment enhanced the ANG-II response, while L-arginine attenuated VP and OT release, thirst, appetite for sodium, antidiuresis, and natriuresis, as well as pressor responses induced by ANG-II.Discussion and conclusionThus, the central nitrergic system participates in the angiotensinergic responses evoked by water deprivation and hypovolemia to refrain neurohypophysial secretion, hydromineral balance, and blood pressure homeostasis.

The association of the plasma vasopressin level during attacks with a prognosis of Meniere's disease

An elevation of the plasma arginine vasopressin (AVP) level has frequently been observed in Meniere's disease patients. However, little is known regarding the mechanism behind this elevation. The plasma AVP levels in acute phase were determined in 21 Meniere's disease patients and 16 patients with other types of vertigo. The plasma AVP levels of Meniere's disease patients in the acute phase were significantly higher than in those of other vertigo patients (p < 0.01). In Meniere's disease patients with abnormally high levels of AVP (more than 3.5 pg/ml) in the acute phase, 36% of patients were resistant to conservative treatments for frequent vertigo attacks for the follow-up period of at least 2years. A significant correlation was observed between the plasma AVP in the acute phase and the highest hearing threshold level at a frequency of 1kHz for the follow-up period of at least 1 year (r=0.45, p < 0.05). These results suggest that the elevation in plasma AVP level in the acute phase is associated with the prognosis of Meniere's disease.SumarioLa elevación del nivel plasmático de vasopresina arginina (AVP) ha sido frecuentemente observado en los pacientes con enfermedad de Meniere. Sin embargo, se sabe poco de los mecanismos detrás de esta elevación. Se determinaron los niveles plasmáticos de AVP durante la fase aguda en 21 paciente con enfermedad de Meniere y en 16 pacientes con otro tipo de vértigo. Los niveles plasmáticos de AVP en los pacientes en la fase aguda de la enfermedad de Meniere fueron significativamente más elevados que aquellos con otro tipo de vértigo (p < 0.01). De los pacientes con enfermedad de Meniere y niveles anormalmente elevados de AVP (más de 5.5 pg/ml) durante la fase aguda, 36% de ellos fueron resistentes al tratamiento conservador para los ataques frecuentes de vértigo en un periodo de seguimiento de hasta 2 años. Se observó una correlación significativa entre el nivel plasmático de AVP en la fase aguda y el umbral más elevado en la frecuencia de 1kHz durante el periodo de seguimiento de un año (r = 0.45, p < 0.05). Estos resultados sugieren que la elevación plasmática de AVP en la fase aguda está asociada con el pronóstico de la enfermedad de Meniere.

Effects of dysfunctional mastication on dynorphin-A nervous system in the amygdala and hippocampus

The effects on vasopressin (VP) release of three dynorphin-A fragments and two antidynorphin antisera were tested in vivo and in vitro.In vivo, the order of potency to inhibit VP release 30 min upon i.c.v. injection was: dynorphin-A-(1–17) > dynorphin-A-(1–13) > dynorphin-A-(1–8).l.c.v. co-administration of 10 nmoles of the specific endopeptidase-inhibitor cFPAAF-pAB and dynorphin-A-(1–8) also suppressed VP secretion. Dynorphin-A-(1–17) antiserum enhanced VP release 20 and 60 min after i.c.v. injection. The antiserum that recognized dynorphin-A-(1–13) elevated VP plasma levels at 60 min post-injection.In vitro, dynorphin-A-(1–8) suppressed electrically evoked VP release from the isolated neuroal lobe. VP release was not affected by dynorphin-A-(1–13), dynorphin-A-(1–17), naloxone, or by the anti-dynorphin antisera.These data indicate that dynorphin-A-(1–17), rather than dynorphin-A-(1–8), plays a role in the centrally located control of neurohypophysial VP release, whereas dynorphin-A-(1–8) is involved in the control located in the posterior pituitary. The synthetic intermediate fragment dynorphin-A-(1–13) appears to affect VP release both centrally and peripherally.

Physiological adaptations of small mammals to desert ecosystems

Adaptations of animals to the xeric environment have been studied in various taxonomic groups and across several deserts. Despite the impressive data that have been accumulated, the focus in most of these studies is mainly on the significance of one variable at a time. Here, we attempt to integrate between responses of several physiological systems, challenged by increasing diet and water salinity and extreme temperatures, acquired in different studies of thermo and osmo-regulatory adaptations, of small rodents, to the xeric environment. Studies have shown differential thermoregulatory responses to increased dietary salinity, which were attributed to habitat and habits of the relevant species. In the thermoregulatory studies, a potential adaptive significance of low metabolic rate was demonstrated. From an evolutionary point of view, the most important adaptation is in the timing of reproduction, as it enables the transfer of genetic properties to the next generation in an unpredictable ecosystem, where reproduction might not occur every year. Results in this aspect show that increased dietary salinity, through an increase in vasopressin plasma levels, plays an important role as a regulator of the reproductive system. We assume that the amount of food existing in the habitat and the amount of reserves in the animal in the form of white adipose tissue are important for reproduction. Photoperiod affects all studied physiological responses, emphasizing the importance of pre-acclimation to seasonal characteristics. We summarize the existing data and suggest neuro-endocrine pathways, which have a central role in these adaptations by affecting thermoregulation, osmoregulation and reproduction to create the optimal response to xeric conditions. These hypotheses can be used as the basis for future studies.

Pressor response to fluid resuscitation in endotoxic shock: Involvement of vasopressin*

To investigate the effects of fluid resuscitation administration on vasopressin secretion and its association with pressor response in endotoxic shock during a period of inappropriately low vasopressin secretion. Prospective, controlled experiment. Animal basic science laboratory. Male Wistar rats, weighing 250 to 300 grams. Rats received lipopolysaccharide (2 mg/kg, intravenous) and had their mean arterial pressure monitored during the next 4 hrs. Subsequently, the animals were assigned randomly to one of seven groups (n = 6 per group) that differed in the composition or volume of the resuscitation fluid administered: control group (no fluid administered); isotonic saline solution (0.9% NaCl; 4 mL/kg); hypertonic saline solution (7.5% NaCl; 4 mL/kg); 0.9% NaCl in 6% hydroxyethyl starch 450/0.7 (4, 8, or 16 mL/kg); or 7.5% NaCl in 6% hydroxyethyl starch 450/0.7 (4 mL/kg). Blood pressure was lower in the lipopolysaccharide-treated group. Administration of 0.9% NaCl in 6% hydroxyethyl starch 450/0.7 did not change mean arterial pressure, but reduced vasopressin plasma levels at a dose of 16 mL/kg. Hypertonic saline solution or 7.5% NaCl in 6% hydroxyethyl starch 450/0.7 administration was followed by an immediate recovery of blood pressure and also by an increase in plasma vasopressin levels when compared to isotonic saline solution. The vasopressin V1 receptor antagonist (10 microg/kg, intravenous, 5 min before infusion) completely blunted the increase in mean arterial pressure induced by hypertonic saline solution or 7.5% NaCl in 6% hydroxyethyl starch 450/0.7 in endotoxemic rats. Isotonic blood volume expansion reduced vasopressin plasma levels. Furthermore, the subsequent release of vasopressin is essential for the pressor response caused by hypertonic fluid infusion during endotoxic shock.

Thymic neuroblastoma with the syndrome of inappropriate secretion of antidiuretic hormone☆

We describe a rare case of thymic neuroblastoma with the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). A 60-year-old male patient was admitted to our hospital for further examination and treatment of anterior mediastinal tumor found at a regular health check-up. On examination there was hyponatremia, decrease in plasma osmolarity and elevation of plasma antidiuretic hormone (ADH) level. Thus, he underwent total thymectomy under the diagnosis of thymoma with SIADH. The tumor was located in the right lobe of the thymus and the final diagnosis was thymic neuroblastoma. To our knowledge, this is the first reported case of thymic neuroblastoma in which production of ADH by tumor cells is demonstrated immunohistochemically. This case highlights the need to consider functional activity of thymic neuroblastoma and complete resection of the tumor is warranted for treatment.

Inhibition of NF-κB ameliorates sepsis-induced downregulation of aquaporin-2/V2receptor expression and acute renal failure in vivo

Acute renal failure (ARF) is frequently associated with polyuria and urine concentration defects and it is a severe complication of sepsis because it increases the mortality rate. Inhibition of NF-kappaB activation has been suggested to provide a useful strategy for the treatment of septic shock. However, the impact on sepsis-induced ARF is still unclear. Therefore, we examined the effect of pyrrolidine dithiocarbamate (PDTC) and of small interfering RNA (siRNA) silencing NF-kappaB p50/p105 on sepsis-induced downregulation of vasopressin V(2) receptors and aquaporin (AQP)-2 channels using a cecal ligation and puncture (CLP) mouse model. CLP caused a time-dependent downregulation of renal vasopressin V(2) receptor and of AQP2 expression without alterations in plasma vasopressin levels. Renal activation of NF-kappaB in response to CLP was attenuated by PDTC pretreatment, which also attenuated the downregulation of V(2) receptor and AQP2 expression. Furthermore, a strong nuclear staining for the NF-kappaB p50 subunit throughout the whole kidney in response to CLP was observed. siRNA against NF-kappaB p50 attenuated the CLP-induced nuclear translocation of the p50 subunit and the CLP-induced downregulation of V(2) receptor and AQP2 expression. Additionally, PDTC and siRNA pretreatment inhibited the CLP-induced increase in renal TNF-alpha and IL-1beta concentration and NOS-2 mRNA abundance. Moreover, PDTC and siRNA pretreatment ameliorated CLP-induced hypotension and ARF. Our findings suggest that NF-kappaB activation is of importance for the downregulation of AQP2 channel and vasopressin V(2) receptor expression during sepsis. In addition, our data indicate that NF-kappaB inhibition ameliorates sepsis-induced ARF.

Magnesium sulphate attenuates arterial pressure increase during laparoscopic cholecystectomy

Magnesium is well known to inhibit catecholamine release and attenuate vasopressin-stimulated vasoconstriction. We investigated whether i.v. magnesium sulphate attenuates the haemodynamic stress responses to pneumoperitoneum by changing neurohumoral responses during laparoscopic cholecystectomy. Thirty-two patients undergoing laparoscopic cholecystectomy were randomly assigned to two groups; a control group was given saline, and a magnesium group received magnesium sulphate 50 mg kg(-1) immediately before pneumoperitoneum. Arterial pressure, heart rate, serum magnesium, plasma renin activity (PRA), and catecholamine, cortisol, and vasopressin levels were measured. Systolic and diastolic arterial pressures were greater in the control group (P<0.05) than in the magnesium group at 10, 20, and 30 min post-pneumoperitoneum. Norepinephrine or epinephrine levels [pg ml(-1), mean (SD)] were higher in the control group than in the magnesium group at 5 [211 (37) vs 138 (18)] or 10 min [59 (19) vs 39 (9)] post-pneumoperitoneum, respectively (P<0.05). In the control group, vasopressin levels [pg ml(-1), mean (SD)] were higher compared with the magnesium group at 5 [64 (18) vs 35 (9), P<0.01] and 10 min [65 (18) vs 47 (11), P<0.05] post-pneumoperitoneum. There were no significant differences between the groups in PRA and cortisol levels. I.V. magnesium sulphate before pneumoperitoneum attenuates arterial pressure increases during laparoscopic cholecystectomy. This attenuation is apparently related to reductions in the release of catecholamine, vasopressin, or both.

Incidence, clinical manifestations, and course of water and electrolyte metabolism disturbances following transsphenoidal pituitary adenoma surgery: a prospective observational study

The authors prospectively studied the incidence, spectrum of clinical manifestations, course, and risk factors of water and electrolyte disturbances (WEDs) following transsphenoidal pituitary adenoma surgery. From the preoperative day to the 14th postoperative day, 57 successive patients undergoing transsphenoidal adenomectomy were monitored daily for body weight, balance of fluids, serum electrolytes, plasma osmolality, plasma antidiuretic hormone (ADH) levels, urinary sodium excretion, urinary osmolality, and subjective sensation of thirst. The type of adenoma operated on and the intraoperative manipulation of the neurohypophysis were also recorded. Fifty-seven patients (mean age 55 years, 61.4% females) harbored 30 clinically hormone-inactive and 27 hormone-secreting pituitary adenomas. Postoperative WED occurred in 75.4% of the patients: in 38.5% as isolated diabetes insipidus (DI); in 21% as isolated hyponatremia; and in 15.7% as combined DI-hyponatremia. The maximum of medians of diuresis (5.750 L) in patients with isolated DI occurred on postoperative Day 2. Nadir of medians of hyponatremia (132 mmol/L) in patients with isolated hyponatremia occurred on postoperative Day 9. In patients with combined DI-hyponatremia, maximum of medians of diuresis (5.775 L) occurred on the 2nd day and nadir of medians of hyponatremia (130 mmol/L) on the 10th postoperative day. Altogether, 8.7% of the patients had to be treated with desmopressin because of DI persisting for >3 months. Of all the patients with hyponatremia, 42.8% were treated by transient fluid-intake restriction due to an IH of <130 mmol/L with or without clinical symptomatology. Transient acute renal failure occurred in one of these patients. Generally, the occurrence of postoperative WEDs was linked to the intraoperative manipulation of the neurohypophysis. Increased thirst correlated significantly with DI (p=0.001 and 0.02, respectively) and decreased thirst with the hyponatremic episode in patients with combined DI-hyponatremia (p=0.003). Decreased urine osmolality correlated significantly with the presence of DI (p=0.023). Electrolyte-free water clearance and urinary Na+ excretion were not correlated with DI and hyponatremia. Antidiuretic hormone was not suppressed during hyponatremia. Water and electrolyte disturbances occurred in the majority of patients undergoing transsphenoidal adenomectomy and were usually transient. Diabetes insipidus is more frequent than hyponatremia. Diabetes insipidus usually occurs during the 1st postoperative day and resolves in the majority of cases within 10 days. In few patients, DI may persist and require therapy with ADH analogs. Hyponatremia usually occurs at the end of the 1st postoperative week and resolves in most cases within 5 days. Very few patients will need treatment other than fluid-intake restriction to avoid serious complications. Thus, careful monitoring of the WEDs in patients undergoing transsphenoidal pituitary adenoma surgery is mandatory for the first 10 postoperative days.

Copeptin, a Surrogate Marker of Vasopressin, Is Associated With Accelerated Renal Function Decline in Renal Transplant Recipients

Chronically elevated vasopressin (VP) plasma levels have been shown to induce accelerated renal function decline in rats with chronic renal failure. Whether endogenous VP is a renal risk factor in humans has not been investigated yet. We aimed to investigate whether, in renal transplant recipients, VP concentration is associated with change in renal function during follow-up. In this prospective study, all consecutive patients visiting our kidney transplant outpatient clinic between August 2001 and July 2003 were asked to participate. Serum creatinine was assessed at baseline and at follow-up. Copeptin, the C-terminal portion of the precursor of VP, was determined at baseline (immunoassay). Univariate and multivariate regression analyses were performed to investigate the association between copeptin and renal function decline. Overall, 548 patients were included 6.0 (2.8-11.6) years after transplantation (men 54%, age 52 [43-60] years). Median follow-up was 3.2 (2.7-3.7) years. Median copeptin level was 9.1 (5.0-18.6) pmol/L at baseline. Copeptin was significantly associated with change in estimated Glomerular Filtration Rate (eGFR; MDRD) during follow-up. When our study population was subdivided according to gender-stratified tertiles of increasing copeptin concentration, mean changes in eGFR during follow-up were -0.03, -0.44, and -1.06 mL/min/1.73 m2 per year. In multivariate regression analysis, the association of copeptin at baseline with change in eGFR during follow-up remained significant after adjustment for age, gender, baseline eGFR, and known risk factors for renal function decline. These findings suggest that in renal transplant patients, VP may play a role in renal function decline.

Plasma Vasopressin and Norepinephrine Profiles Predict Outcome in Septic Patients with Impaired Compensatory Mechanisms

Objective: The objective of this study is to evaluate the role of plasma vasopressin/norepinephrine ratios in disclosing masked septic shock. Methods: A prospective sample of consecutive patients visiting the emergent department of a university teaching hospital and meeting the criteria of sepsis was enrolled. Besides sepsis work-up, we measured plasma vasopressin and norepinephrine concentrations and their ratios to detect the occurrence of septic shock in those with impaired compensatory mechanisms. Results: Of 284 patients with sepsis, forty-five aged from 45 to 92 years old met the inclusive criteria during a 12-month period (from January 2007 to December 2007). Three categories were classified as those with septic shock (n=12), those with severe sepsis (n=22) and those with only sepsis (n=11) according to 6-hour outcome. Plasma vasopressin and norepinephrine concentrations were measured. The plasma vasopressin level measured before the final outcome was significantly lower for those with septic shock (septic shock group, 3.8±0.9 pg/mL [95% CI 3.2-4.4 pg/mL]; severe sepsis group, 19.3±3.5 pg/mL [95% CI 17.5-20.8 pg/mL]; sepsis group 10.2±3.2 pg/mL [95% CI 8.2-12.2 pg/mL], P＜0.001) whereas the norepinephrine level highest for the same group (septic shock group, 3,490±410 pg/mL [95% CI 3,215-3,765 pg/mL]; severe sepsis group, 3,290±558 pg/mL [95% CI 3,043-3, 537 pg/mL]; and sepsis group, 1,854±427 pg/mL [95% CI 1,562-2,146 pg/mL]). At a cut-off value of 5 pg/mL, the sensitivity and specificity of plasma vasopressin in diagnosing septic shock are 100% (95% CI [71%-100%]) and 97 (95% CI [85%-99%])%, respectively. At a cut-off value of 2,750 pg/mL, the sensitivity and specificity of plasma norepinephrine in diagnosing septic shock are 100% (95% CI [71%-100%]) and 47% (95% CI [30%-65%]), respectively. The vasopressin/norepinephrine ratio had a sensitivity of 97% (95% CI [91%-100%]) and a specificity of 82% (95% CI [76%-88%]) at a cut-off value of vasopressin / norepinephrine of 1.0×10^(-3). Conclusions: Plasma vasopressin/norepinephrine profiles can provide accurate prediction of impending septic shock and outcome for the patients with impaired compensatory mechanisms.

Levels of vasopressin and oxytocin in neurohypophysis and plasma of the postnatally developing rat and the influence of hypothyroidism on rat fetuses.

Arginine vasopressin (AVP) and oxytocin (OXT) were measured simultaneously by radioimmunoassay in neurohypophyses of rats immediately before birth (fetal day 22) onward to day 50 of life. The neurohypophysial content of AVP exceeded that of OXT by factor 17 at fetal day 22, by 20 immediately post natum, and by 2 at day 21 of life, respectively. As compared to day 0, the content at day 21 is considerably higher (AVP 24 fold, OXT 270 fold). The poor correlation between neurohypophysial AVP and OXT content suggests the possibility of a different onto-genetic development of both neuropeptide systems. Both AVP and OXT were detected in pooled rat plasma at various postnatal stages. Hypo- and hyperthyroidism induced experimentally during gestation did not result in a significant change in neuropeptide content of fetal neural lobes.