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P. Smits - One of the best experts on this subject based on the ideXlab platform.
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Effects of Arginine Vasopressin and 1-desamino-8-D Arginine Vasopressin on forearm vasculature of healthy subjects and patients with a V2 receptor defect
Journal of Hypertension, 1995Co-Authors: A.f. Van Lieburg, Nine V A M Knoers, L.a.h. Monnens, P. SmitsAbstract:OBJECTIVES: To assess which Vasopressin receptor subtype mediates the vasodilation occurring in response to Arginine Vasopressin and 1-desamino-8-D (DD)-Arginine Vasopressin and whether nitric oxide is involved in these effects. MATERIALS AND METHODS: Vasoactive effects of Arginine Vasopressin and DD-Arginine Vasopressin on forearm vasculature were studied in healthy subjects and in patients with congenital nephrogenic diabetes insipidus with a Vasopressin type 2 (V2) receptor gene defect. Venous occlusion plethysmography was used to assess the forearm blood flow responses to the infusion of Arginine Vasopressin and its analogue into the brachial artery, in the presence and the absence of the nitric oxide synthase inhibitor L-NG-monomethyl-Arginine (L-NMMA). RESULTS: In healthy subjects (n =10), DD-Arginine Vasopressin (0.1, 1 and 10 or 5, 10 and 20 ng/min per dl) induced a dose-related increase in forearm blood flow, but did not affect forearm blood flow in the patients with nephrogenic diabetes insipidus (n = 3). In two healthy subjects, seven increasing doses of Arginine Vasopressin (0.25-12 ng/min per dl) induced an initial decrease in forearm blood flow and then a gradual increase. In one of the patients, the same Arginine Vasopressin doses produced a persistent decrease in forearm blood flow. In the healthy subjects, infusion of L-NMMA reduced forearm blood flow significantly (n = 10). Subsequent administration of DD-Arginine Vasopressin during L-NMMA infusion produced a slight reduction in the forearm blood flow increase compared with DD-Arginine Vasopressin alone, but this was significant only for the absolute forearm blood flow increase induced by 10 ng/min per dl in all subjects. Infusion of Arginine Vasopressin in the presence of L-NMMA did not increase forearm blood flow significantly. CONCLUSIONS: In human forearm vasculature, extrarenal V2 receptors mediate the vasodilation induced by DD-Arginine Vasopressin or high doses of Arginine Vasopressin, whereas these receptors are not necessary for Arginine Vasopressin-induced vasoconstriction. The DD-Arginine Vasopressin-induced vasodilation seems to be mediated predominantly by a mechanism other than endothelial nitric oxide release, whereas Arginine Vasopressin-induced vasodilation seems to involve nitric oxide release only.
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Effects of Arginine Vasopressin and 1-desamino-8-D Arginine Vasopressin on forearm vasculature of healthy subjects and patients with a V2 receptor defect.
Journal of hypertension, 1995Co-Authors: A.f. Van Lieburg, Nine V A M Knoers, L.a.h. Monnens, P. SmitsAbstract:To assess which Vasopressin receptor subtype mediates the vasodilation occurring in response to Arginine Vasopressin and 1-desamino-8-D (DD)-Arginine Vasopressin and whether nitric oxide is involved in these effects. Vasoactive effects of Arginine Vasopressin and DD-Arginine Vasopressin on forearm vasculature were studied in healthy subjects and in patients with congenital nephrogenic diabetes insipidus with a Vasopressin type 2 (V2) receptor gene defect. Venous occlusion plethysmography was used to assess the forearm blood flow responses to the infusion of Arginine Vasopressin and its analogue into the brachial artery, in the presence and the absence of the nitric oxide synthase inhibitor L-NG-monomethyl-Arginine (L-NMMA). In healthy subjects (n =10), DD-Arginine Vasopressin (0.1, 1 and 10 or 5, 10 and 20 ng/min per dl) induced a dose-related increase in forearm blood flow, but did not affect forearm blood flow in the patients with nephrogenic diabetes insipidus (n = 3). In two healthy subjects, seven increasing doses of Arginine Vasopressin (0.25-12 ng/min per dl) induced an initial decrease in forearm blood flow and then a gradual increase. In one of the patients, the same Arginine Vasopressin doses produced a persistent decrease in forearm blood flow. In the healthy subjects, infusion of L-NMMA reduced forearm blood flow significantly (n = 10). Subsequent administration of DD-Arginine Vasopressin during L-NMMA infusion produced a slight reduction in the forearm blood flow increase compared with DD-Arginine Vasopressin alone, but this was significant only for the absolute forearm blood flow increase induced by 10 ng/min per dl in all subjects. Infusion of Arginine Vasopressin in the presence of L-NMMA did not increase forearm blood flow significantly. In human forearm vasculature, extrarenal V2 receptors mediate the vasodilation induced by DD-Arginine Vasopressin or high doses of Arginine Vasopressin, whereas these receptors are not necessary for Arginine Vasopressin-induced vasoconstriction. The DD-Arginine Vasopressin-induced vasodilation seems to be mediated predominantly by a mechanism other than endothelial nitric oxide release, whereas Arginine Vasopressin-induced vasodilation seems to involve nitric oxide release only.
Michael G Ross - One of the best experts on this subject based on the ideXlab platform.
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chronic in utero plasma hyperosmolality alters hypothalamic Arginine Vasopressin synthesis and pituitary Arginine Vasopressin content in newborn lambs
American Journal of Obstetrics and Gynecology, 2002Co-Authors: Bernice A Ramirez, Shengbiao Wang, Nathash Kallichanda, Michael G RossAbstract:Abstract Objective: Arginine Vasopressin is synthesized in the hypothalamus and secreted by the posterior pituitary gland in response to plasma hypertonicity. Previous studies suggest that in utero and neonatal exposure of rat pups to prolonged alterations of plasma osmolality may permanently alter (imprint) Arginine Vasopressin synthesis and secretion, thus adult responses to osmotic challenges. Little is known, however, of the potential for imprinting of neuroendocrinologic systems in precocial species. In view of the frequent occurrence of altered maternal and fetal plasma tonicity (eg, maternal dehydration, hyperemesis), we sought to determine the effect of prolonged maternal hypertonicity on Arginine Vasopressin gene expression and pituitary gland content in neonatal sheep. Study Design: Pregnant ewes at 119 ± 3 days of gestation were water restricted to achieve and maintain plasma hypertonicity (10-20 mOsm/kg above baseline level) until normal term delivery. Newborns were provided maternal nursing ad libitum. Within 24 hours after birth, study neonatal lambs (n = 6) and age-matched control neonatal lambs (n = 5) were killed, and the pituitary gland and hypothalamus were removed and frozen immediately. Pituitary Arginine Vasopressin content was determined by radioimmunoassay, and hypothalamic Arginine Vasopressin gene expression was quantified with Northern blot. Differences in pituitary Arginine Vasopressin content and hypothalamic Arginine Vasopressin gene expression (Arginine Vasopressin/ β-actin ratio) between study and control newborn lambs were analyzed by unpaired t test. Results: In response to maternal water restriction, maternal plasma osmolality increased from 307 ± 0.9 mOsm/kg to 325 ± 1.3 mOsm/kg, and plasma sodium increased from 147 ± 1.3 mEq/L to 156 ± 1.2 mEq/L. The maternal plasma hyperosmolality and hypernatremia were maintained until normal term delivery. At the time of death, study (in utero dehydrated) lambs had higher plasma sodium (150 ± 0.4 mEq/L vs 146.5 ± 1.5 mEq/L; P P P P P Conclusion: Despite the presence of plasma hypernatremia, prolonged elevation of fetal plasma tonicity increases newborn pituitary Arginine Vasopressin content yet decreases hypothalamic Arginine Vasopressin gene expression. The present study suggests that prolonged prenatal exposure to plasma hypertonicity may imprint the hypothalamic-pituitary Arginine Vasopressin regulatory system. (Am J Obstet Gynecol 2002;187:191-6.)
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Regulation of hypothalamic Arginine Vasopressin messenger ribonucleic acid and pituitary Arginine Vasopressin content in fetal sheep: Effects of acute tonicity alterations and fetal maturation
American journal of obstetrics and gynecology, 1998Co-Authors: Xiaohui Zhao, Mark J Nijland, M. Gore Ervin, Michael G RossAbstract:Abstract Objective: Fetal Arginine Vasopressin contributes to fetal and amniotic fluid homeostasis by increasing water resorption in the kidney and, at higher plasma levels, circulatory homeostasis by vasopressor effects. In utero and neonatal exposure of rat pups to prolonged alterations in plasma osmolality may permanently alter (imprint) pituitary Arginine Vasopressin content and adult responses to osmotic challenges. Our objective was to investigate fetal developmental changes and the impact of maternal dehydration and maternal hyponatremia on fetal pituitary Arginine Vasopressin content and hypothalamic Arginine Vasopressin messenger ribonucleic acid expression. Study Design: Ten pregnant ewes with singleton fetuses (135 ± 1 day) were chronically prepared with maternal vascular catheters. Ewes were assigned to receive water deprivation ( n = 4) [desamino, d -Arg8]-Arginine Vasopressin–induced plasma hyponatremia ( n = 3), or 4 days of observation ( n = 3). Three additional pregnant ewes with preterm (110 ± 1 day) singleton fetuses were also included for a study of maturational effects. Daily maternal blood samples were analyzed for determination of plasma Arginine Vasopressin, electrolytes, and osmolality. After the study protocol, fetuses were operatively delivered, umbilical blood samples obtained, and fetuses put to death for pituitary and hypothalamic tissues. Pituitary Arginine Vasopressin content was determined by radioimmunoassay, and hypothalamus Arginine Vasopressin messenger ribonucleic acid expression was detected by Northern blotting. Results: Dehydration significantly ( P r 2 = 0.563; P = .02). Arginine Vasopressin messenger ribonucleic acid expression was significantly lower in both preterm and near-term fetuses ( P P P Conclusions: The significant inverse relation between Arginine Vasopressin content and Arginine Vasopressin messenger ribonucleic acid suggests a dynamic Arginine Vasopressin synthesis–content feedback relationship is functional in the near-term fetus. Although relatively acute periods of maternal hypertonicity or hypotonicity do not alter fetal pituitary Arginine Vasopressin content or hypothalamic Arginine Vasopressin messenger ribonucleic acid expression, longer-term plasma tonicity alterations may potentially have an impact on the fetal Arginine Vasopressin hypothalamic-pituitary axis. (Am J Obstet Gynecol 1998;179:899-905.)
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treatment of oligohydramnios with maternal 1 deamino 8 d Arginine Vasopressin induced plasma hypoosmolality
American Journal of Obstetrics and Gynecology, 1996Co-Authors: Michael G Ross, Mark J Nijland, Leonard Cedars, Anthony OgundipeAbstract:Abstract OBJECTIVE: Maternal 1-deamino-[8-D-Arginine] Vasopressin (a selective antidiuretic agonist) and oral water loading decrease maternal and fetal plasma osmolality and markedly increase fetal urine flow in sheep. We hypothesized that a titrated reduction in maternal plasma osmolality would increase human amniotic fluid volume. STUDY DESIGN: Pregnant women ( n = 5) with oligohydramnios at term were administered oral water loading (20 ml/kg) and intravenous 1-deamino-[8-D-Arginine] Vasopressin (2 μ g) to induce antidiuresis. Maternal plasma and urine osmolality and urine production were measured hourly, and water replacement was titrated for 8 hours to reduce plasma osmolality by 15 to 20 mOsm/kg. The amniotic fluid index determined by ultrasonography was measured at baseline, 8 hours, and 24 hours. A control group of pregnant women ( n = 5) with oligohydramnios at term was observed for 8 hours with maintenance intravenous hydration. RESULTS: In 1-deamino-[8-D-Arginine] Vasopressin - treated women, maternal urine flow increased with oral water loading, decreased with 1-deamino-[8-D-Arginine] Vasopressin administration, and remained reduced for 8 hours. Maternal plasma osmolality significantly decreased (285 ± 4 to 265 ± 4 mOsm/kg) and the amniotic fluid index significantly increased (4.1 ± 0.6 to 8.2 ± 1.5 cm) at 8 hours. Although maternal urine osmolality returned to basal values at 24 hours, plasma osmolality was reduced and the amniotic fluid index remained significantly increased (8.2 ± 1.3 cm). There was no change in the amniotic fluid index (4.3 ± 0.4 to 4.7 ± 0.7 cm) in control patients observed with maintenance intravenous hydration. CONCLUSIONS: Maternal 1-deamino-[8-D-Arginine] Vasopressin and oral water administration can reduce and stabilize plasma osmolality and increase amniotic fluid volume. 1-Deamino-[8-D-Arginine] Vasopressin therapy has potential for the prevention and treatment of oligohydramnios. (AM J OBSTET GYNECOL 1996;174:1608-13.)
Simon W. Lam - One of the best experts on this subject based on the ideXlab platform.
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Arginine Vasopressin for the treatment of septic shock in adults.
Pharmacotherapy, 2010Co-Authors: Seth R. Bauer, Simon W. LamAbstract:Sepsis remains one of the leading causes of mortality in the United States. Cardiovascular compromise is one of the major contributors to the high mortality associated with sepsis. Current cardiovascular support in patients with septic shock involves fluid administration, use of catecholamines, and potentially the use of inotropes, corticosteroids, or Arginine Vasopressin. Vasopressin is an endogenous hormone essential for both osmotic and cardiovascular homeostasis. Various studies have suggested that exogenous administration of Arginine Vasopressin may be an effective adjunctive therapy to traditional catecholamines for the management of hypotension during septic shock. Of particular interest is the Vasopressin and Septic Shock Trial (VASST), which found no mortality benefit when comparing the addition of Arginine Vasopressin to norepinephrine versus continuous dose increases in norepinephrine alone. However, results of the a priori subgroup and post hoc analyses of this trial suggest that patients may benefit if Arginine Vasopressin is used in patients with less severe shock, defined as those receiving a relatively low norepinephrine-equivalent dose of 5-14 μg/minute, or in those at risk for renal failure. Current guidelines from the Surviving Sepsis Campaign recommend Arginine Vasopressin 0.03 unit/minute may be added to norepinephrine with the anticipation of an effect equal to higher doses of norepinephrine alone. Many practitioners continue to utilize Arginine Vasopressin for patients with septic shock due to its mechanisms of benefit on pathophysiologic derangements in this disease. Clinicians must be knowledgeable about the use of Arginine Vasopressin in septic shock, including controversial areas where guidelines do not always provide concrete recommendations.
Yasuyoshi Ouchi - One of the best experts on this subject based on the ideXlab platform.
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Identification of Arginine Vasopressin mRNA in rat aortic smooth muscle cells.
Biochemical and biophysical research communications, 1997Co-Authors: Koichiro Nagano, Kenji Toba, Masahiro Akishita, Koichi Kozaki, Masato Eto, Masayoshi Hashimoto, Noriko Sudoh, Masao Yoshizumi, Yasuyoshi OuchiAbstract:Abstract We investigated the expression of mRNA for Arginine Vasopressin in vascular smooth muscle cells and A10 cells using reverse transcription–polymerase chain reaction and Northern blot analysis. Arginine Vasopressin mRNA was identified both in rat aortic smooth muscle cells and A10 cells, suggesting that Arginine Vasopressin is locally produced in vascular smooth muscle cells. Arginine Vasopressin, a potent vasoconstrictor, may modulate vascular function in an autocrine or paracrine fashion.
Martin W. Dünser - One of the best experts on this subject based on the ideXlab platform.
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Influences of hydrocortisone therapy on Arginine Vasopressin plasma levels in septic shock.
Wiener Klinische Wochenschrift, 2011Co-Authors: Stefan Jochberger, Martin W. DünserAbstract:Concomitant hydrocortisone and Arginine Vasopressin therapy increases Arginine Vasopressin plasma levels and may improve survival in septic shock. The objective of this post hoc analysis of a prospective study was to determine whether hydrocortisone therapy increases Arginine Vasopressin plasma levels in patients with septic shock. Forty-five patients were included into the study, of whom 23 (51.1%) received a hydrocortisone infusion because of escalating vasopressor dosages. Median Arginine Vasopressin plasma levels did not differ between patients treated with and without hydrocortisone therapy [4.2 (2.2–6.2) vs. 4.3 (2.7–6.1) pmol/L] both in a bivariate (p = 0.43, Mann–Whitney U-test) and a logistic regression model adjusted for differences in disease severity (p = 0.38). No association was further detected between hydrocortisone therapy and Arginine Vasopressin plasma levels in an adjusted linear regression model [β-coefficient, –0.57 (–1.86–0.73), p = 0.39]. We conclude that increased Arginine Vasopressin plasma levels during concomitant Arginine Vasopressin and hydrocortisone therapy in septic shock result from reduced Arginine Vasopressin clearance and not increased Arginine Vasopressin secretion or interaction of hydrocortisone with the Arginine Vasopressin assay.
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Arginine Vasopressin in vasodilatory shock: effects on metabolism and beyond.
Current opinion in anaesthesiology, 2008Co-Authors: Martin W. Dünser, Martin WestphalAbstract:PURPOSE OF REVIEW: To describe the effects of Arginine Vasopressin other than its vasoconstrictive and antidiuretic potential in vasodilatory shock. RECENT FINDINGS: Arginine Vasopressin influences substrate metabolism by stimulation of hepatic glucose release, gluconeogenesis, ureogenesis and fatty acid esterification. Although Arginine Vasopressin is a secretagogue of different hormones, only prolactin increases during Arginine Vasopressin therapy. Plasmatic and cellular coagulation are affected by Arginine Vasopressin, resulting in thrombocyte aggregation. Therefore, platelet count typically decreases following Arginine Vasopressin infusion in critically ill patients. In addition, Arginine Vasopressin reduces bile flow and may increase bilirubin concentrations. Despite its potential to decrease serum sodium, no change in electrolytes was observed in critically ill patients receiving Arginine Vasopressin. Although Arginine Vasopressin is an endogenous antipyretic, body temperature is not decreased by central venous Arginine Vasopressin infusion. In addition, Arginine Vasopressin modulates immune function through V1 receptors. Compared with norepinephrine, Arginine Vasopressin may have protective effects on endothelial function. Net Arginine Vasopressin effects on gastrointestinal motility seem to be inhibitory and are dose dependent. SUMMARY: Except for its antidiuretic and vasoconstrictive actions, the effects of Arginine Vasopressin in patients with vasodilatory shock have so far only been partially examined. Potential influences of Arginine Vasopressin on metabolism and immune, liver and mitochondrial function remain to be assessed in future studies.
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Arginine Vasopressin in 316 patients with advanced vasodilatory shock
Critical Care Medicine, 2005Co-Authors: Gunter Luckner, Martin W. Dünser, Volker Wenzel, Stefan Jochberger, Viktoria D Mayr, Hanno Ulmer, Stefan Schmid, Hans Knotzer, Werner Pajk, Walter R HasibederAbstract:Objective:To assess the effects of Arginine Vasopressin (AVP) on hemodynamic, clinical, and laboratory variables and to determine its adverse side effects in advanced vasodilatory shock.Design:Retrospective study.Patients:A total of 316 patients.Interventions:AVP infusion (4 units/hr).Measurements a
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Management of vasodilatory shock: defining the role of Arginine Vasopressin.
Drugs, 2003Co-Authors: Martin W. Dünser, Volker Wenzel, Andreas Mayr, W. HasibederAbstract:The rationale for an Arginine Vasopressin (argipressin) infusion was put forward after it was discovered that patients in shock states might have an endogenous Arginine Vasopressin deficiency. Subsequently, several investigations impressively demonstrated that Arginine Vasopressin can successfully stabilise haemodynamics even in advanced vasodilatory shock. We report on physiological and pharmacological aspects of Arginine Vasopressin, and summarise current clinical knowledge on employing a continuous Arginine Vasopressin infusion in critically ill patients with catecholamine-resistant vasodilatory shock of different aetiologies. In view of presented experimental evidence and current clinical experience, a continuous Arginine Vasopressin infusion of ∼2 to ∼6 IU/h can be considered as a supplemental strategy to vasopressor catecholamines in order to preserve cardiocirculatory homeostasis in patients with advanced vasodilatory shock. Because data on adverse effects are still limited, Arginine Vasopressin should be reserved for patients in whom adequate haemodynamic stabilisation cannot be achieved with conventional vasopressor therapy or who have obvious adverse effects of catecholamines that result in further significant haemodynamic deterioration. For the same reasons, Arginine Vasopressin should not be used as a single, alternative vasopressor agent instead of catecholamine vasopressors. Future prospective studies will be necessary to define the exact role of Arginine Vasopressin in the therapy of vasodilatory shock.