Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “VASOPRESSIN”

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

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

At least 631 records · Page 35Linked to original sources
PubMed1993

Transgenic mouse models of vasopressin expression.

Arginine vasopressin is a nine-amino acid neuropeptide hormone important in the regulation of water metabolism. It also may have a role in other physiological functions, such as blood pressure regulation and the response to stress. Whole animal studies have provided a good understanding of vasopressin physiology and regulation of the normal vasopressin gene, and in vitro cell culture studies have demonstrated important features of the intracellular regulation of vasopressin gene expression. Transgenic mice provide useful models for the study of the in vivo regulation of gene expression. Previously reported mouse lines transgenic with vasopressin gene constructs have not expressed the transgene in a tissue distribution similar to that detected for the endogenous mouse vasopressin gene. An 8.2-kb genomic construct of the rat vasopressin gene, including 3 kb each of 5' and 3' flanking sequences, has been used to develop a line of transgenic mice. These animals express the transgene in a tissue-specific manner, demonstrate appropriate osmotic regulation of transgenic vasopressin mRNA, and have normal water metabolism. Animals homozygous for the 8.2-kb transgene have increased basal plasma levels of vasopressin peptide but have no apparent change in basal water metabolism. The findings with this and other previously reported mouse lines transgenic for vasopressin constructs provide a basis for developing future transgenic lines to study the in vivo regulation of the vasopressin gene.

Animals↗
PubMed2001

Vasopressin-induced protein kinase C-dependent superoxide generation contributes to atp-sensitive potassium channel but not calcium-sensitive potassium channel function impairment after brain injury.

BACKGROUND AND PURPOSE: Pial artery dilation in response to activators of the ATP-sensitive K(+) (K(ATP)) and calcium-sensitive K(+) (K(Ca)) channels is impaired after fluid percussion brain injury (FPI). Vasopressin, when coadministered with the K(ATP) and K(Ca) channel agonists cromakalim and NS1619 in a concentration approximating that observed in cerebrospinal fluid (CSF) after FPI, blunted K(ATP) and K(Ca) channel-mediated vasodilation. Vasopressin also contributes to impaired K(ATP) and K(Ca) channel vasodilation after FPI. In addition, protein kinase C (PKC) activation generates superoxide anion (O(2)(-)), which in turn contributes to K(ATP) channel impairment after FPI. We tested whether vasopressin generates O(2)(-) in a protein kinase C (PKC)-dependent manner, which could link vasopressin release to impaired K(ATP) and K(Ca) channel-induced pial artery dilation after FPI. METHODS: Injury of moderate severity (1.9 to 2.1 atm) was produced with the lateral FPI technique in anesthetized newborn pigs equipped with a closed cranial window. Superoxide dismutase-inhibitable nitroblue tetrazolium (NBT) reduction was determined as an index of O(2)(-) generation. RESULTS: Under sham injury conditions, topical vasopressin (40 pg/mL, the concentration present in CSF after FPI) increased superoxide dismutase-inhibitable NBT reduction from 1+/-1 to 23+/-4 pmol/mm(2). Chelerythrine (10(-7) mol/L, a PKC inhibitor) blunted such NBT reduction (1+/-1 to 9+/-2 pmol/mm(2)), whereas the vasopressin antagonist l-(beta-mercapto-beta,beta-cyclopentamethylene propionic acid)2-(o-methyl)-Tyr-arginine vasopressin (MEAVP) blocked NBT reduction. Chelerythrine and MEAVP also blunted the NBT reduction observed after FPI (1+/-1 to 15+/-1, 1+/-1 to 4+/-1, and 1+/-1 to 5+/-1 pmol/mm(2) for sham-, chelerythrine-, and MEAVP-treated animals, respectively). Under sham injury conditions, vasopressin (40 pg/mL) coadministered with cromakalim or NS1619 blunted dilation in response to these K(+) channel agonists, whereas chelerythrine partially restored such impaired vasodilation for cromakalim but not NS1619. Cromakalim- and NS1619-induced pial artery dilation also was blunted after FPI. MEAVP partially protected dilation to both K(+) channel agonists after FPI, whereas chelerythrine did so for only cromakalim responses (for cromakalim at 10(-8) and 10(-6) mol/L, 13+/-1% and 23+/-1%, 2+/-1% and 5+/-1%, 9+/-1% and 15+/-2%, and 9+/-1% and 16+/-2% for sham-, FPI-, FPI-MEAVP-, and FPI-chelerythrine-pretreated animals, respectively). CONCLUSIONS: These data show that vasopressin, in concentrations present in CSF after FPI, increased O(2)(-) production in a PKC-dependent manner and contributes to such production after FPI. These data show that vasopressin contributes to K(ATP) but not K(Ca) channel function impairment in a PKC-dependent manner after FPI and suggest that vasopressin contributes to K(Ca) channel function impairment after FPI via a mechanism independent of PKC activation.

Adenosine Triphosphate↗
PubMed2006

Vasopressin improves outcome in out-of-hospital cardiopulmonary resuscitation of ventricular fibrillation and pulseless ventricular tachycardia: a observational cohort study.

INTRODUCTION: An increasing body of evidence from laboratory and clinical studies suggests that vasopressin may represent a promising alternative vasopressor for use during cardiac arrest and resuscitation. Current guidelines for cardiopulmonary resuscitation recommend the use of adrenaline (epinephrine), with vasopressin considered only as a secondary option because of limited clinical data. METHOD: The present study was conducted in a prehospital setting and included patients with ventricular fibrillation or pulseless ventricular tachycardia undergoing one of three treatments: group I patients received only adrenaline 1 mg every 3 minutes; group II patients received one intravenous dose of arginine vasopressin (40 IU) after three doses of 1 mg epinephrine; and patients in group III received vasopressin 40 IU as first-line therapy. The cause of cardiac arrest (myocardial infarction or other cause) was established for each patient in hospital. RESULTS: A total of 109 patients who suffered nontraumatic cardiac arrest were included in the study. The rates of restoration of spontaneous circulation and subsequent hospital admission were higher in vasopressin-treated groups (23/53 [45%] in group I, 19/31 [61%] in group II and 17/27 [63%] in group III). There were also higher 24-hour survival rates among vasopressin-treated patients (P < 0.05), and more vasopressin-treated patients were discharged from hospital (10/51 [20%] in group I, 8/31 [26%] in group II and 7/27 [26%] group III; P = 0.21). Especially in the subgroup of patients with myocardial infarction as the underlying cause of cardiac arrest, the hospital discharge rate was significantly higher in vasopressin-treated patients (P < 0.05). Among patients who were discharged from hospital, we found no significant differences in neurological status between groups. CONCLUSION: The greater 24-hour survival rate in vasopressin-treated patients suggests that consideration of combined vasopressin and adrenaline is warranted for the treatment of refractory ventricular fibrillation or pulseless ventricular tachycardia. This is especially the case for those patients with myocardial infarction, for whom vasopressin treatment is also associated with a higher hospital discharge rate.

Adult↗
PubMed1984

Vasopressin concentration in amniotic fluid as an index of fetal hypoxia: mechanism of release in sheep.

Hypoxia is a potent stimulus to the release of vasopressin in fetal sheep and, in turn, plasma concentrations of the hormone correlate inversely with fetal oxygenation. Because the fetal kidney contributes to vasopressin clearance, we propose that measurement of increased amounts of vasopressin in amniotic fluid would be indicative of fetal hypoxia. We therefore measured concentrations of vasopressin in amniotic fluid under resting conditions, during and after fetal hypoxia, and with intravenous and intra-amniotic administration of vasopressin in 15 chronically instrumented fetal lambs 111-141 d gestation. In the resting state mean (+/- SE) vasopressin concentrations in amniotic fluid (1.6 +/- 0.3 pg . ml-1) did not differ from those in maternal (1.4 +/- 0.4 pg . ml-1) or fetal (1.8 +/- 0.2 pg . ml-1) plasma. After exposure of the ewe to 10% O2 or partial occlusion of the umbilical cord, vasopressin concentrations in fetal plasma increased significantly (P less than 0.001) to 200 +/- 59 pg . ml-1 with a delayed increase in amniotic fluid concentrations (P less than 0.03) to 15.8 +/- 4.5 pg . ml-1. This rise in concentration of vasopressin in amniotic fluid was sustained for at least 24 h and levels at that time were highly correlated with peak plasma concentrations (r = 0.83, P less than 0.001). Intravenous infusion of vasopressin into the fetus was accompanied by an equally significant (P less than 0.02) and sustained increase of vasopressin in amniotic fluid. After intraamniotic injection of vasopressin, levels remained increased for at least 24 h.(ABSTRACT TRUNCATED AT 250 WORDS)

Amniotic Fluid↗
PubMed1984

Vasopressin concentration in amniotic fluid as an index of fetal hypoxia: mechanism of release in sheep.

Hypoxia is a potent stimulus to the release of vasopressin in fetal sheep, and plasma concentrations of the hormone correlate inversely with fetal oxygenation. Since the fetal kidney contributes to vasopressin clearance, we propose that measurement of increased amounts of vasopressin in amniotic fluid would be indicative of fetal hypoxia. Therefore, we measured concentrations of vasopressin in amniotic fluid under resting conditions, during and after fetal hypoxia, and with intravenous and intra-amniotic administration of vasopressin in 15 chronically instrumented fetal lambs between 111 and 141 days gestation. In the resting state, mean (+/- SE) vasopressin concentrations in amniotic fluid (1.6 +/- 0.3 pg ml-1) did not differ from those in maternal (1.4 +/- 0.4 pg ml-1) or fetal (1.8 +/- 0.2 pg ml-1) plasma. Following exposure of the ewe to 10% O2 or partial occlusion of the umbilical cord, vasopressin concentrations in fetal plasma increased significantly (P less than 0.001) to 200 +/- 59 pg ml-1 with a delayed increase in amniotic fluid concentrations (P less than 0.03) to 15.8 +/- 4.5 pg ml-1. This rise in concentration of vasopressin in amniotic fluid was sustained for at least 24 h and levels at that time were highly correlated with peak plasma concentrations (r = 0.83; P less than 0.001). Intravenous infusion of vasopressin into the fetus was accompanied by an equally significant (P less than 0.02) and sustained increase of vasopressin in amniotic fluid. Following intra-amniotic injection of vasopressin, levels remained increased for at least 24 h.(ABSTRACT TRUNCATED AT 250 WORDS)

Amniotic Fluid↗
PubMed1991

Adrenocorticotropin and cortisol responses to vasopressin during pregnancy.

CRH is secreted by the placenta into the maternal and fetal circulation during pregnancy in humans and non-human primates. ACTH and cortisol responses to exogenous CRH are blunted during pregnancy. In the present study we examined the pituitary-adrenal response to another corticotropin releasing factor, vasopressin. Studies were performed in chronically catheterized female baboons moving freely in their home cages; 13 studies were performed in 4 pregnant animals, and 8 studies were performed in 6 nonpregnant animals. Vasopressin was administered iv in 2 doses (0.3 and 3.0 U), and plasma samples were obtained for CRH, ACTH, and cortisol measurements. Results are expressed as the mean +/- SEM. Baseline plasma CRH was 240 +/- 20 pmol/L in the pregnant animals and unmeasurable (less than 20) in the nonpregnant animals. In the pregnant animals, ACTH concentrations rose from a baseline of 6.4 +/- 1.3 pmol/L to 10.1 +/- 0.4 after 0.3 U vasopressin and to 24.9 +/- 5.2 after 3.0 U vasopressin. In the nonpregnant animals, ACTH levels were 5.8 +/- 1.3 at baseline, 6.7 +/- 1.3 after the 0.3-U dose, and 14.6 +/- 2.4 after the 3.0-U dose. The peak ACTH response after each dose of vasopressin was higher in the pregnant animals than in the nonpregnant animals (P less than 0.05). The baseline cortisol level in the pregnant animals was 960 +/- 80 nmol/L and rose to 1370 +/- 110 and 1535 +/- 165 after the 2 doses of vasopressin, respectively. The baseline cortisol concentration in the nonpregnant animals was 910 +/- 86 nmol/L. The cortisol level was 990 +/- 75 after the 0.3-U vasopressin dose and 1380 +/- 140 after the 3.0-U dose. The peak cortisol response after the 0.3-U dose was significantly higher in the pregnant animals (P less than 0.02), while the peak cortisol responses after the 3.0-U dose were similar in the 2 groups of animals. In a single animal, vasopressin was administered sequentially at 4 gestational ages during pregnancy and then 2 times in the postpartum period. The ACTH response to vasopressin increased as pregnancy progressed and then decreased in the postpartum period. In summary, the ACTH and cortisol responses to 0.3 and 3.0 U vasopressin, iv, are enhanced during pregnancy in the baboon, although the responses to exogenous CRH are blunted during gestation. We conclude that the chronic placental CRH stimulation of the pituitary-adrenal axis during pregnancy leads to an enhanced response to vasopressin and a down-regulation of the response to exogenous CRH.

Adrenocorticotropic Hormone↗
PubMed1992

Plasma and cerebrospinal fluid measures of arginine vasopressin secretion in patients with bulimia nervosa and in healthy subjects.

Bulimia nervosa is a psychiatric syndrome associated with intense hunger, deficient satiety mechanisms, an obsessional preoccupation with the adverse consequences of eating, ritualistic binge eating, and subsequent purging to forestall the effects of the binge. The morbidity of this illness reflects both the psychological suffering associated with a life organized around pathological eating behaviors, as well as medical complications such as fluid and electrolyte imbalances that occur largely as a result of purging and laxative abuse. We report here a study of the osmoregulation of plasma arginine vasopressin secretion and of vasopressin levels in the cerebrospinal fluid. This study was undertaken because vasopressin not only functions as the antidiuretic hormone, and thus as a principal modulator of fluid and electrolyte balance, but also because, in animals, centrally directed vasopressin delays the extinction of behaviors acquired during aversive conditioning. Thirteen normal-weight female patients with bulimia nervosa were studied after at least 1 month of nutritional stabilization and supervised abstinence from binge eating and purging. Plasma vasopressin, plasma sodium, and subjective thirst were measured serially before and during a 2-h infusion of 3% hypertonic saline (0.1 ml/kg min). In addition, cerebrospinal fluid was obtained by lumbar puncture upon admission and at 1 week before hypertonic saline infusion in 11 of these patients and in an additional 11 female patients who did not participate in the hypertonic infusion study. Fifteen healthy normal weight individuals (4 female, 11 male) served as controls for the hypertonic saline infusion and a separate group of 11 healthy normal weight female controls underwent puncture. Compared to controls, bulimic subjects showed a significant reduction in the plasma vasopressin response to hypertonic saline; in 12/13, plasma vasopressin correlated closely with plasma sodium, whereas in one patient vasopressin fluctuated erratically, with no relation to plasma sodium. Cerebrospinal fluid vasopressin levels were significantly higher in patients, and correlated positively with basal thirst level, which was enhanced in bulimics. Compared to controls, patients showed significant polyuria. We conclude that patients with bulimia nervosa have abnormal levels of vasopressin in their plasma and cerebrospinal fluid during abstinence from binge eating and purging. The disturbance in osmoregulation may aggravate the maintenance of adequate fluid volume in these patients, while the increase in centrally directed vasopressin may have relevance to their obsessional preoccupation with the aversive consequences of eating and weight gain.

Adult↗
PubMed2004

Fixed-dose vasopressin compared with titrated dopamine and norepinephrine as initial vasopressor therapy for septic shock.

STUDY OBJECTIVE: To investigate the early blood pressure effects of vasopressin compared with titrated catecholamines as initial drug therapy in patients with septic shock. DESIGN: Retrospective cohort, single-center study. SETTING: Intensive care units at the Mayo Clinic, Rochester, Minnesota. PATIENTS: Fifty, 49, and 51 intensive care patients treated initially with vasopressin, norepinephrine, and dopamine, respectively. INTERVENTION: Patients received either intravenous infusion of fixed-dose vasopressin 0.04 U/minute or titrated infusions of norepinephrine or dopamine for low systemic arterial pressures. MEASUREMENTS AND MAIN RESULTS: Patients treated with vasopressin, norepinephrine, and dopamine were similar in all measured characteristics except for their score on the Acute Physiology and Chronic Health Evaluation (APACHE) III (dopamine > vasopressin, p=0.049), renal comorbidities (dopamine > vasopressin, p=0.03) and baseline mean arterial pressure (MAP) (norepinephrine < vasopressin, p=0.005 or dopamine < vasopressin, p=0.05). In all patients, MAP 1 hour before and 1 hour afte intervention, heart rate, and systolic blood pressure were obtained. No treatment differences were identified in achieving postvasopressin MAP after adjusting for APACHE III score, renal dysfunction, and baseline MAP. In patients receiving vasopressin, 28-day mortality was 52%, similar to those receiving norepinephrine (65%, p=0.28) and dopamine (60%, p=0.53). CONCLUSION: Initial, fixed-dose vasopressin infusions increased MAP to 70 mm Hg or greater at 1 hour in intensive care patients with septic shock, similar to titrated norepinephrine or dopamine. Fixed-dose vasopressin appears appropriate as an alternative agent for hemodynamic support in patients with septic shock.

APACHE↗
PubMed1986

Vasopressin secretion in normotensive black and white men and women on normal and low sodium diets.

The plasma concentration and the 24-h urinary excretion of vasopressin were studied in normal black and white men and women on a normal sodium (150 mmol/day) diet for 3 days and a low sodium (9 mmol/day; furosemide, 1 mg/kg on first day) diet for 4 days. During the normal sodium diet, the 24-h urinary excretion of vasopressin was significantly (P less than 0.05) higher in men than in women and higher (P less than 0.05) in black than in white subjects. Corresponding differences in plasma vasopressin concentrations (P less than 0.05 to 0.01) were observed, with the exception that the difference between white men and women was not statistically significant. These data suggest that under basal conditions the secretion of vasopressin is higher in men and black subjects than in women and white subjects, although differences in the metabolic clearance of vasopressin cannot be ruled out. Reduction in sodium intake resulted in a significantly (P less than 0.01) decreased excretion of vasopressin in all groups except black women, but had no effect on plasma vasopressin concentrations. Significant (P less than 0.01) differences with respect to sex and race persisted for vasopressin excretion, but not for plasma vasopressin concentrations. Sex- and race-related differences in vasopressin could not be attributed to differences in blood pressure, plasma volume or plasma sodium concentration. The physiological consequences of these differences in vasopressin remain to be determined.

Black People↗
PubMed1990

Mechanism of the inhibition of protein synthesis by vasopressin in rat liver.

A recent study reported that protein synthesis was inhibited in rat livers perfused with medium containing vasopressin (Chin, K. -V., Cade, C., Brostrom, M. A., and Brostrom, C. O. (1988) Int. J. Biochem. 20, 1313-1319). The inhibition of protein synthesis caused by vasopressin was associated with a disaggregation of polysomes, suggesting that peptide chain initiation was slowed relative to elongation. In contrast, Redpath and Proud (Redpath, N. T., and Proud, C. G. (1989) Biochem. J. 262, 69-75) recently reported an inhibition of peptide chain elongation by a calcium/calmodulin-dependent mechanism. Therefore, the question remained whether only peptide chain initiation was inhibited or both initiation and elongation were affected by vasopressin. In the present study, vasopressin was found to inhibit protein synthesis in both perfused rat livers and isolated rat hepatocytes. Ribosomal half-transit times in isolated hepatocytes averaged 1.9 +/- 0.1 min with or without vasopressin present in the media, demonstrating that the rate of peptide chain elongation was unaffected by vasopressin. Instead, the inhibition of protein synthesis induced by vasopressin was manifested at the level of peptide chain initiation. Vasopressin treatment resulted in both a 2-fold increase in the number of free ribosomal particles and a greater than 50% decrease in the amount of [35S]methionine bound to 43 S preinitiation complexes. In addition, the activity of eukaryotic initiation factor (eIF) 2B in crude extracts from perfused livers was reduced to 53% of the control value in response to vasopressin. The inhibition of eIF-2B activity was associated with an increase in the proportion of the alpha-subunit of eIF-2 in the phosphorylated form from 9.6% in control livers to 30.7% in livers perfused with medium containing vasopressin. The results demonstrate the novel finding that the inhibition of protein synthesis in vasopressin-treated livers is caused by a reduction in eIF-2B activity due to an increase in phosphorylation of eIF-2 alpha.

Animals↗
PubMed1987

Nicotine-induced release of vasopressin in the conscious rat: role of opioid peptides and hemodynamic effects.

Nicotine has been shown to stimulate the release of vasopressin and to cause significant hemodynamic changes. The mechanisms leading to enhanced vasopressin secretion and the vascular consequences of the high plasma vasopressin levels during nicotine infusion have not yet been determined. Therefore, the purposes of the present study were 1) to examine in normal conscious rats the role of opioid peptides in the nicotine-induced increase in plasma vasopressin levels and 2) to assess the role of vasopressin in the hemodynamic effects of nicotine (20 micrograms/min for 15 min) using a specific V1 antagonist of the vascular actions of vasopressin. Plasma vasopressin levels were significantly increased in the nicotine-treated animals (39.5 +/- 10 vs. 3.7 +/- 0.6 pg/ml in the controls, P less than .01). Pretreatment with naloxone, an antagonist of opioids at their receptors, did not reduce the vasopressin levels (47.7 +/- 9 pg/ml). Nicotine also increased mean blood pressure (122.5 +/- 2.5 to 145.2 +/- 3.3 mm Hg, P less than .01) and decreased heart rate (461 +/- 6 to 386 +/- 14.5 beats/min, P less than .05). Administration of the vasopressin V1 antagonist before the nicotine infusion did not affect the systemic hemodynamics or the regional blood flow distribution, as assessed by radiolabeled microspheres. Thus, these results suggest that the nicotine-induced secretion of vasopressin is not mediated by opioid receptors and that the high plasma vasopressin levels do not exert any significant hemodynamic effect on cardiac output or blood flow distribution.

Animals↗
PubMed1981

Vasopressin secretion in primary polydipsia and cranial diabetes insipidus.

Vasopressin secretion was studied in a group of 18 patients with polydipsia (urine volume greater than 21/24 h) in whom nephrogenic diabetes insipidus had been excluded. Osmoregulation of vasopressin release was defined by hypertonic saline infusion, and three independent non-osmotic tests of vasopressin release were also applied. A wide spectrum of abnormalities in vasopressin secretion was observed. Four patients seem to have primary polydipsia, since they showed a normal response to osmotic stimulation, but non-osmotic vasopressin release was subnormal in two. The remaining 14 patients had cranial diabetes insipidus, as judged by subnormal or absent vasoprsssin responses to hypertonic saline infusion. Of these 14, five had undetectable vasopressin during osmotic stimulation, but each mounted a response to the non-osmotic stimuli; three of these had familial polyuria. Three further patients appeared to have isolated osmoreceptor defects, showing normal responses to non-osmotic stimuli but none to osmotic stress. Four patients with partial cranial diabetes insipidus, as judged by subnormal vasopressin response to osmotic stimuli, seemed to have normal osmoreceptor function but deficient vasopressin release. There was no correlation between the degree of vasopressin response to osmotic stimuli and the three non-osmotic tests of vasopressin release, and in particular vasopressin release should not replace osmotic tests to define cranial diabetes insipidus.

Adult↗
PubMed1993

Relationship of the antihypertensive effect of vasopressin withdrawal to sodium excretion in the Doca-salt hypertensive rat.

Arterial pressure, sodium excretion, urine output, and plasma atrial natriuretic peptide (ANP) concentrations were measured before, during, and after a 3-h i.v. infusion of arginine-vasopressin (vasopressin; 20 ng/kg/min) in conscious Doca-salt hypertensive rats. Arterial pressure was 166 +/- 8 mm Hg before the infusion of vasopressin; in comparison, pressure was only 130 +/- 4 mm Hg 5 h after stopping the infusion. The fall in pressure after withdrawal of an equipressor dose of phenylephrine in hypertensive animals was much less. In sham normotensive rats, pressure did not fall below control levels after stopping either the vasopressin or phenylephrine infusion. Sodium excretion rates were higher during infusions of vasopressin than during phenylephrine infusions. However, the elevations observed during vasopressin were similar in the hypertensive (25.3 +/- 4.9 mumol/kg/min) and normotensive (22.9 +/- 2.7 mumol/kg/min) groups. Urinary output increased to a greater extent in the hypertensive rats during the infusions of both vasopressin and phenylephrine, but the increases were similar for the 2 pressor agents. Plasma levels of ANP were elevated during the infusions of vasopressin in the normotensive rats, but not in hypertensive rats. The results indicate that the fall in pressure associated with cessation of a pressor dose of vasopressin appears specific to the hypertensive state, and relatively specific to vasopressin. This withdrawal-induced antihypertensive phenomenon (WAP) does not appear to be due solely to the preceding natriuresis and diuresis during the infusion of vasopressin. However, because the hypertensive animal may be more sensitive to a given degree of sodium loss, the possibility that the natriuresis could play a contributing or permissive role cannot be excluded.

Animals↗
PubMed1997

A prospective randomized trial of arginine vasopressin in the treatment of vasodilatory shock after left ventricular assist device placement.

BACKGROUND: Vasodilatory shock requiring catecholamine pressors occurs in some patients following cardiopulmonary bypass. Prompted by a clinical observation, we investigated the use of vasopressin as a treatment for this syndrome in a randomized, controlled trial. METHODS AND RESULTS: Patients undergoing placement of a left ventricular assist device (n=23) were evaluated for post-bypass vasodilatory shock requiring catecholamine pressors, and consecutive eligible subjects (n=10) were evenly randomized to blinded intravenous vasopressin or saline placebo. Vasopressin (0.1 U/min) increased mean arterial pressure (57+/-4 to 84+/-2 mm Hg, P<.001) and systemic vascular resistance (813+/-113 to 1188+/-87 dyne-s/cm5, P<.001), with decreased norepinephrine administration. There was no significant response to saline, but in three subjects who crossed over, blinded vasopressin increased mean arterial pressure (69+/-8 to 93+/-4 mm Hg) and systemic vascular resistance (898+/-88 to 1443+/-72 dyne-s/cm5) with decreased norepinephrine administration. Plasma vasopressin concentrations prior to randomization clustered in two groups: one (n=5) with concentrations inappropriately low for the degree of hypotension (8.4+/-2.1 pg/mL) and a second (n=3) with moderately elevated levels (33.7+/-1.6 pg/mL); vasopressin increased mean arterial pressure in the low vasopressin group from 57+/-4 to 85+/-2 mm Hg (P<.01) and in the high vasopressin group from 68+/-8 to 86+/-4 mm Hg. CONCLUSIONS: Vasopressin is an effective pressor in vasodilatory shock after cardiopulmonary bypass. An absolute vasopressin deficiency was observed in the majority of patients, but all subjects responded to vasopressin administration.

Arginine Vasopressin↗
PubMed1998

[Identification of metabolic pathways of brain angiotensin II and angiotensin III: predominant role of angiotensin III in the control of vasopressin secretion].

Angiotensin (Ang) II and AngIII are two peptide effectors of the brain renin-angiotensin system that participate in the control of blood pressure and increase water consumption and vasopressin release. In an attempt to delineate the respective roles of these peptides in the regulation of vasopressin secretion, their metabolic pathways and their effects on vasopressin release were identified in vivo. For this purpose, we used recently developed selective inhibitors of aminopeptidase A (APA) and aminopeptidase N (APN), two enzymes that are believed to be responsible for the N-terminal cleavage of AngII and AngIII, respectively. Mice received [3H]AngII intracerebroventricularly (i.c.v.) in the presence or absence of the APA inhibitor, EC33 ((S)-3-amino-4-mercapto-butylsulfonate de sodium) or the APN inhibitor, EC27 ((S)-2-amino-pentan-1,5-dithiol). [3H]AngII and [3H]AngIII levels were evaluated from hypothalamus homogenates by HPLC. EC33 increased the half-life of [3H]AngII 2.6-fold and completely blocked the formation of [3H]AngIII, whereas EC27 increased the half-life of [3H]AngIII 2.3-fold. In addition, the effects of EC33 and EC27 on Ang- induced vasopressin release were studied in mice. AngII was injected i.c.v. in the presence or absence of EC33, and plasma vasopressin levels were estimated by RIA. While vasopressin levels were increased 2-fold by AngII, EC33 inhibited AngII-induced vasopressin release in a dose-dependent manner. In contrast, EC27 injected alone increased in a dose-dependent manner vasopressin levels. The EC27-induced vasopressin release was completely blocked by the coadministration of the Ang receptor antagonist (Sar1-Ala8) AngII. These results demonstrate for the first time that i) APA and APN are involved in vivo in the metabolism of brain AngII and AngIII, respectively, and that ii) the action of AngII on vasopressin release depends upon the prior conversion of AngII to AngIII. This shows that AngIII behaves as one of the main effector peptides of the brain renin-angiotensin system in the control of vasopressin release.

Aminopeptidases↗
PubMedDate not supplied

Characterization of intrathecal vasopressin-induced antinociception, scratching behavior, and motor suppression.

Intrathecal (IT) administration of vasopressin produces antinociception, scratching behavior, and motor suppression. The present experiments characterized these effects with regards to the following: 1) VP receptor specificity, 2) possible involvement of endogenous opiates, 3) possible involvement of seizure activity, and 4) whether the antinociception is due to direct actions of VP at the spinal cord. These studies showed that IT administration of a V1-specific vasopressin antagonist completely blocked the antinociception, scratching behavior, and motor suppression produced by 25 ng IT vasopressin. Furthermore, IT administration of the vasopressin metabolite, [pGlu4,Cyt6]AVP(4-9), produced none of the effects produced by vasopressin. Systemic administration of the opiate antagonists naloxone (1 mg/kg IP) and naltrexone (10 mg/kg IP) had no significant effect on the antinociception produced by IT vasopressin, whereas naltrexone potentiated the scratching behavior. Neither the IT vasopressin-induced antinociception nor scratching behavior was affected by pretreatment with the anticonvulsant sodium valproate. In addition, IT vasopressin inhibited the tail flick reflex in rats with transected spinal cords, demonstrating direct spinal effects of vasopressin. In conclusion, IT administration of vasopressin produces antinociception, scratching behavior, and motor suppression via activation of VP-specific receptors in the spinal cord.

Animals↗
PubMed1990

Role of vasopressin in renal vascular changes with hypoxemia and hypercapnic acidosis in conscious dogs.

To evaluate the role of vasopressin in the renal changes during combined acute hypoxemia and acute hypercapnic acidosis, eight conscious female mongrel dogs prepared with controlled sodium intake at 80 meq/24 h for 4 days were studied in one of the following six protocols: acute hypoxemia (80 min, arterial PO2 34 +/- 1 mmHg) followed by combined acute hypoxemia and hypercapnic acidosis (40 min, arterial PO2 35 +/- 1 mmHg, arterial PCO2 58 +/- 1 mmHg, pH = 7.20 +/- 0.01) during 1) intrarenal vehicle at 0.5 ml/min (N = 8); or 2) intrarenal infusion of vasopressin V1-receptor antagonist [d(CH2)5Tyr(Me)]AVP at 5 ng.kg-1.min-1 (N = 5); and with normal gas exchange during 3) intrarenal vasopressin at 0.05 mU.kg-1.min-1 (N = 8); 4) simultaneous infusion of intrarenal vasopressin and [d(CH2)5Tyr(Me)]AVP, 5 ng.kg-1.min-1 (N = 4); 5) intrarenal [d(CH2)5Tyr(Me)]AVP, 5 ng.kg-1.min-1 (N =4); and 6) intrarenal vehicle at 0.5 ml/min (N = 7). Intrarenal infusion of a subpressor dose of vasopressin resulted in a transient decrease in glomerular filtration rate and effective renal plasma flow over the first 20 min of infusion, suggesting that vasopressin induced nonsustained vasoconstriction of the renal vasculature. Intrarenal administration of [d(CH2)5Tyr-(Me)]AVP failed to block the fall in glomerular filtration rate or effective renal plasma flow when renal arterial blood vasopressin levels were elevated by intrarenal administration of exogenous vasopressin or by elevated systemic arterial endogenous circulating vasopressin during combined acute hypoxemia and hypercapnic acidosis. These data suggest that vasopressin (V1-receptor stimulation) does not play an important role in the renal vasoconstriction during combined acute hypoxemia and hypercapnic acidosis in conscious dogs.

Acidosis↗
PubMed1986

Solubilization of the vasopressin receptor from rat liver plasma membranes. Evidence for a receptor X GTP-binding protein complex.

The GTPase activity of plasma membranes isolated from rat livers was stimulated 20% over basal by vasopressin. A concentration dependency curve showed that maximal stimulation was obtained with 10(-8) M vasopressin. The vasopressin-stimulated GTPase activity was not inhibited in plasma membranes that had been ADP-ribosylated with either cholera toxin or pertussis toxin. Identical results were obtained from plasma membranes that had been solubilized with 1% digitonin. When membranes that had been solubilized after preincubation with [3H]vasopressin were subjected to sucrose gradient centrifugation, the majority of protein-bound [3H]vasopressin migrated as a single band with a sedimentation constant of 16.8 S. Moreover, there was a GTPase activity that migrated with the bound [3H]vasopressin. This peak of bound [3H]vasopressin was decreased by 90% when the sucrose gradient centrifugation was run in the presence of 10 microM guanosine 5'-O-(thiotriphosphate). When the 16.8 S peak of bound [3H]vasopressin was further purified over a wheat germ lectin-Sepharose column, a GTPase activity co-eluted from the column with the protein-bound [3H]vasopressin. Direct evidence that a GTP-binding protein was present in the 16.8 S peak was obtained by the immunodetection of a 35-kDa beta subunit of a GTP-binding protein. These results support the conclusion that liver plasma membranes contain a GTP-binding protein that can complex with the vasopressin receptor.

Adenosine Diphosphate Ribose↗