Low Plasma Arginine Vasopressin Research Articles

Nephrogenic Syndrome of Inappropriate Antidiuresis

Mutations in the vasopressin V2 receptor gene are responsible for two human tubular disorders: X-linked congenital nephrogenic diabetes insipidus, due to a loss of function of the mutant V2 receptor, and the nephrogenic syndrome of inappropriate antidiuresis, due to a constitutive activation of the mutant V2 receptor. This latter recently described disease may be diagnosed from infancy to adulthood, as some carriers remain asymptomatic for many years. Symptomatic children, however, typically present with clinical and biological features suggesting inappropriate antidiuretic hormone secretion with severe hyponatremia and high urine osmolality, but a low plasma arginine vasopressin level. To date, only two missense mutations in the vasopressin V2 receptor gene have been found in the reported patients. The pathophysiology of the disease requires fuller elucidation as the phenotypic variability observed in patients bearing the same mutations remains unexplained. The treatment is mainly preventive with fluid restriction, but urea may also be proposed.

Relative deficiency of arginine vasopressin in children after cardiopulmonary bypass*

To describe changes in plasma arginine vasopress in concentration in children following cardiopulmonary bypass and determine whether, in some patients, plasma arginine vasopressin remains relatively low despite hemodynamic instability. Prospective observational study. Pediatric intensive care unit at a tertiary care university hospital. One hundred twenty patients ≤ 18 yrs of age undergoing open heart surgery requiring cardiopulmonary bypass at Children's Hospital of Michigan between January 2008 and January 2009. Blood samples were collected before cardiopulmonary bypass and 4, 24, and 48 hrs after cardiopulmonary bypass for measurement of plasma arginine vasopressin concentration. Mean plasma arginine vasopressin (pg/mL) for all patients was 21 ± 63 before cardiopulmonary bypass and 80 ± 145, 43 ± 79, and 19 ± 25 at 4, 24, and 48 hrs, respectively, after cardiopulmonary bypass. Patients with plasma arginine vasopressin below the lower quartile (< 9.2 pg/mL) at 4 hrs after cardiopulmonary bypass (n = 29), labeled group A, were examined separately and compared with the rest of the study population, labeled group B. Mean plasma arginine vasopressin was 4.9 ± 2.6 in group A at 4 hrs after cardiopulmonary bypass, statistically unchanged from its baseline mean plasma arginine vasopressin of 5.0 ± 10.4 (p = .977). Mean plasma arginine vasopressin in group B was 104 ± 160 at 4 hrs after cardiopulmonary bypass. Mean plasma arginine vasopressin of group A was also significantly lower as compared with group B before and 24 and 48 hrs after cardiopulmonary bypass. Hemodynamics, inotrope score, and serum sodium did not differ between groups at any time point. Plasma arginine vasopressin was measured immediately before exogenous arginine vasopressin administration in 10 patients; only those (n = 3) with hemodynamic instability and relatively low plasma arginine vasopressin concentration (< 9.2 pg/mL) had notable hemodynamic improvement. In some children undergoing open heart surgery, plasma arginine vasopressin concentration is relatively low at baseline and remains low after cardiopulmonary bypass regardless of hemodynamic stability and serum osmolality. These children are likely the optimal candidates for exogenous arginine vasopressin should hemodynamic compromise occur.

Plasma arginine vasopressin concentration in horses undergoing surgery for colic

To determine if horses before undergoing anesthesia for surgical correction of colic would have lower plasma arginine vasopressin (AVP) concentrations than healthy horses undergoing anesthesia for arthroscopic surgery, and would not increase their plasma AVP concentrations in response to anesthesia and surgery. Prospective clinical study. University teaching hospital. Fourteen horses with colic and 8 healthy horses. Horses with colic underwent anesthesia and surgery for alleviation of colic, and healthy horses underwent anesthesia and surgery for arthroscopy. Plasma AVP was measured perioperatively in horses with colic and in healthy horses. Before anesthesia, and 30 and 60 minutes after induction, horses with colic had greater median plasma AVP concentrations than control horses (P<or=0.001); thereafter during anesthesia differences in AVP concentrations between the 2 groups were not significant. In the control group, plasma AVP concentration increased during 120 minutes of anesthesia; no such increase occurred in colic horses. Compared with healthy horses, horses with colic had higher preanesthesia plasma AVP concentrations that did not increase further in response to anesthesia and surgery. Exogenous AVP is associated with decreased splanchnic perfusion in a variety of animal species and, therefore, could be detrimental to horses with colic. Thus, it may be inappropriate to use exogenous AVP in support of blood pressure in anesthetized horses with colic. Further studies are warranted to define appropriate indications for the use of AVP in horses with colic.

AT1a receptor knockout in mice impairs urine concentration by reducing basal vasopressin levels and its receptor signaling proteins in the inner medulla

Angiotensin II plays an important role in the regulation of blood pressure, body salt and fluid balance, and urine concentration. Mice with deletion of the AT(1a) receptor develop polyuria and urine concentration defects. We studied the mechanisms of these urine concentration defects by treating wild-type and AT(1a)-knockout mice with arginine vasopressin (AVP) for 2 weeks, controlling their water intake, or giving them an osmotic diuretic (sucrose) in order to determine whether central or nephrogenic mechanisms were involved. Under basal conditions, AT(1a)-knockout mice were hypotensive, had lower plasma AVP, and excreted more urine with a markedly reduced osmolality compared with wild-type mice. However, basal glomerular filtration rates were similar in both strains of mice. We isolated total lysate and membrane proteins from the inner medulla of wild-type and mutant mouse kidneys, and found that the amounts of aquaporin 2 (AQP2), adenylyl cyclases III and V/VI, and phosphorylated MAP kinases ERK 1/2 proteins were all reduced in the inner medulla of the knockout mice. Infusion of AVP raised plasma levels and blood pressure proportionally in both strains, but polyuria persisted and urine osmolality remained significantly lower in the knockout mice. Although AVP increased urine osmolality slightly in water-deprived knockout mice, this was well below the basal osmolality of wild-type mice. The diuretic response to the hyperosmotic sucrose was also impaired in the knockout mice. Neither AVP nor water rationing restored the levels of the inner medullary signaling proteins and membrane AQP2 proteins in the knockout mice. We suggest that AT(1a) receptor deletion causes polyuria and urine concentration defects by decreasing basal AVP release and impairing AVP-induced receptor signaling in the inner medulla.

Effect of Administration of Corticotropin-Releasing Hormone and Glucocorticoid on Arginine VasopressinResponse to Osmotic Stimulus in Normal Subjects and Patients with Hypocorticotropinism without Overt Diabetes Insipidus

We examined the effect of CRH administration on the response of plasma arginine vasopressin (AVP) induced by an osmotic stimulus in six normal subjects and five patients with hypocorticotropinism without overt diabetes insipidus (four patients with Sheehan's syndrome and one with idiopathic pituitary dwarfism with ACTH deficiency). Hypertonic saline infusion (855 mmol/L saline solutions at a rate of 205 mumol/kg.min for 10 min) increased plasma AVP 5.7-fold (P less than 0.01) in normal subjects and 2.4-fold (P less than 0.05) in the patients. CRH administration significantly augmented the plasma AVP response to the osmotic stimulus in the normal subjects, but not in the patients with hypocorticotropinism. CRH administration alone did not influence plasma AVP. These findings suggest that a central CRH-related mechanism(s) was at least partly involved in the augmentation of AVP release. Based on the relatively low plasma AVP response to the osmotic stimulus in patients and their lower plasma AVP levels and higher plasma osmolality under basal conditions, we suggest that patients with hypocorticotropinism have partial diabetes insipidus, in which impairment of central CRH action might be, at least in part, involved. The response of plasma AVP to the osmotic stimulus was attenuated significantly when the patients were given cortisol. Since basal PRA, plasma aldosterone, plasma osmolality, hematocrit, body weight, mean blood pressure, and heart rate were similar with and without cortisol administration, this effect of cortisol may have been due to central suppression of the AVP response to the osmotic stimulus.

Effect of arginine vasopressin on urine formation and plasma atrial natriuretic peptide level in conscious dogs

We investigated the relationship between plasma arginine vasopressin (AVP) and atrial natriuretic peptide (ANP) levels and urine formation in conscious dogs. The rate of urine production and urinary electrolyte excretion were determined following infusion of high doses of AVP to dogs in different volume states. Water deprivation for 24 h induced an antidiuresis while the plasma osmolality, plasma AVP and plasma ANP remained at physiological levels. Subsequent i.v. administration of AVP did not alter the production of urine. Oral water loading (20 ml/kg body weight) induced low plasma AVP levels (1.3 ± 0.5 pg/ml, mean ± S.E.M.). Following AVP administration to the water-loaded group, the urine production rate decreased significantly from baseline while the osmolality of the urine increased significantly. Plasma ANP levels did not differ significantly between the two experimental groups, and did not change following i.v. administration of AVP. The results show that, in conscious dogs. (1) the production of a small volume of highly concentrated urine can occur with plasma AVP levels of below 5 pg/ml, (2) 24 h of dehydration induces an antidiuresis while plasma peptides, as well as the different biochemical variables, remain within normal limits, (3) increased plasma AVP levels do not induce a change in plasma ANP levels under these experimental conditions, (4) infusion of AVP induces a significantly increased K + excretion but only in overhydrated animals.

Variable arginine vasopressin levels in neonatal congestive heart failure

Arginine vasopressin levels in 17 neonates with cardiac disease were compared with control levels in 10 healthy newborn infants. Infants with congestive heart failure who were free of left ventricular outflow tract obstruction had a mean level of 80 ± 18 pg/ml, which was significantly greater than the mean control level (p < 0.001). Infants with congestive heart failure and left ventricular outflow tract obstruction had a mean vasopressin level of 3 ± 0.7 pg/ml, which was lower than the mean control level of 6 ± 0.7 pg/ml (p < 0.05).The data suggest that impaired forward flow to high pressure sinoaortic and ventricular baroreceptors is necessary for vasopressin release in congestive heart failure. In left ventricular outflow tract obstruction with heart failure these receptors may be impaired or absent, leading to decreased vasopressin release. Low plasma arginine vasopressin may adversely affect circulatory homeostasis.

Development of a cytochemical assay for plasma vasopressin: application to studies on water loading normal man.

A cytochemical assay has been developed to measure human plasma arginine vasopressin. It is based on the stimulation of Na+-K+, ATPase activity located in the outer medulla of the rat kidney, and is capable of detecting very low plasma arginine vasopressin concentrations, limit of detection 0.01 pmol/l. Specificity for vasopressin stimulation of the enzyme is conferred on the assay by the use of specific vasopressin antiserum. Index of precision of the assay is 0.21. Degradation of arginine vasopressin in plasma in inhibited by phenanthroline. Samples may be stored up to 8 weeks at -70 degrees C. Intra- and inter-assay coefficients of variation were 22% (n = 8) and 104% (n = 12), respectively. A sustained water load in eight healthy male adults caused a fall in plasma osmolality from a basal of 286.5 +/- 2.0 (mean +/- SEM) to 279.2 +/- 2.4 mmol/kg after the load (P less than 0.001), which was associated with a reduction in urine osmolality from 867 +/- 54 to 69 +/- 3 mmol/kg. Plasma immunoreactive arginine vasopressin fell from 1.3 +/- 0.3 pmol/l to become undetectable (less than 0.3 pmol/l), but plasma cytochemical arginine vasopressin decreased from 0.96 +/- 0.14 to 0.07 +/- 0.02 pmol/l. There was a curvilinear relationship between plasma osmolality and plasma cytochemical arginine vasopressin, which militated against the concept of an osmotic threshold for vasopressin release.