Oestradiol acts through its beta receptor to increase vasopressin neuronal activation and secretion induced by dehydration.

Vasopressinergic neurones of the supraoptic (SON) and paraventricular (PVN) nuclei express oestrogen receptor (ER)ß and receive afferent projections from osmosensitive neurones that express ERα. However, which subtype of these receptors mediates the effects of oestradiol on vasopressin (AVP) secretion induced by hydromineral challenge has not yet been demonstrated in vivo. Moreover, AVP secretion induced by hyperosmolality is known to involve activation of TRPV1 (transient receptor potential vanilloid, member 1) in magnocellular neurones, although whether oestradiol modulates expression of this receptor is unknown. Thus, the present study aimed to clarify the mechanisms involved in the modulation exerted by oestradiol on AVP secretion, specifically investigating the involvement of ERß, ERα and TRPV1 receptors in response to water deprivation (WD). We observed that treatment with an ERß agonist potentiated AVP secretion and vasopressinergic neuronal activation induced by WD. This increase in AVP secretion induced by WD was reversed by an ERß antagonist. By contrast to ERß, the ERα agonist did not alter plasma AVP concentrations or activation of AVP neurones in the SON and PVN. Additionally, Fos expression in the subfornical organ was not altered by the ERα agonist. TRPV1 mRNA expression was increased by WD in the SON, although this response was not altered by any treatment. The results of the present study suggest that ERß mediates the effects of oestradiol on AVP secretion in response to WD, indicating that the effects of oestradiol occur directly in AVP neurones without affecting TRPV1.

[Small cell lung cancer associated with multiple paraneoplastic syndromes].

We report the case of a patient presenting with multiple severe electrolyte disturbances who was subsequently found to have small cell lung cancer. Upon further evaluation, she demonstrated three distinct paraneoplastic processes, including the syndrome of inappropriate antidiuretic hormone, Fanconi syndrome, and an inappropriate elevation in fibroblast growth factor-23 (FGF23). The patient underwent one round of chemotherapy, but she was found to have progressive disease. After 36 days of hospitalization, the patient made the decision to enter hospice care and later she expired.

Small cell lung cancer associated with multiple paraneoplastic syndromes / Cáncer de pulmón de células pequeñas asociado a múltiples síndromes paraneoplásicos

Abstracts We report the case of a patient presenting with multiple severe electrolyte disturbances who was subsequently found to have small cell lung cancer. Upon further evaluation, she demonstrated three distinct paraneoplastic processes, including the syndrome of inappropriate antidiuretic hormone, Fanconi syndrome, and an inappropriate elevation in fibroblast growth factor-23 (FGF23). The patient underwent one round of chemotherapy, but she was found to have progressive disease. After 36 days of hospitalization, the patient made the decision to enter hospice care and later she expired.

Resumen Se reporta el caso de una paciente que ingresó al hospital para evaluación de múltiples trastornos electrolíticos y, posteriormente, se le hizo el diagnóstico de cáncer de pulmón de células pequeñas. Tras la evaluación médica, se detectaron tres síndromes paraneoplásicos: síndrome de secreción inadecuada de hormona antidiurética, síndrome de Fanconi y elevación inapropiada del factor 23 de crecimiento de fibroblastos. Se le administró quimioterapia sin éxito, por lo cual se decidió darle tratamiento paliativo y, un tiempo después, falleció.

Differential effects of osmotic and SSR149415 challenges in maternally separated and control rats: the role of vasopressin on spatial learning.

Maternal separation (MS) has been demonstrated to up-regulate the hypothalamic vasopressin (VP) system. Intracerebrally released VP has been demonstrated to affect several types of animal behaviour, such as active/passive avoidance, social recognition, and learning and memory. However, the role of VP in spatial learning remains unclear. In the present study, we investigated the effects of an osmotic challenge and a V1b receptor-specific (V1bR) antagonist, SSR149415, on spatial learning of maternally separated and animal facility reared (AFR) adult male Wistar rats. The osmotic challenge was applied by injecting a hypertonic saline solution, 1h before the Morris water maze test (MWM). V1bR antagonist SSR149415 (5mg/kg) was injected i.p. twice (1h and 30 min) previous to the MWM. A combined treatment with both osmotic challenge and the SSR149415 was applied to the third group whereas rats for basal condition were injected with isotonic saline. Under basal condition no differences between AFR and MS groups were observed. MS rats showed severe impairment during the MWM after the osmotic challenge, but not after the administration of SSR149415. For AFR rats, the opposite phenomenon was observed. The joint application of SSR149415 and osmotic challenge restored the spatial learning ability for both groups. The differential impairment produced by osmotic stress-induced up-regulation and SSR149415 induced V1bR blockage in MS and control rats suggested that VP involvement in spatial learning depends on the individual intrinsic ligand-receptor functional state.

Cardiovascular effects of the intracerebroventricular injection of adrenomedullin: roles of the peripheral vasopressin and central cholinergic systems

Our objective was to investigate in conscious Sprague-Dawley (6-8 weeks, 250-300 g) female rats (N = 7 in each group) the effects of intracerebroventricularly (icv) injected adrenomedullin (ADM) on blood pressure and heart rate (HR), and to determine if ADM and calcitonin gene-related peptide (CGRP) receptors, peripheral V1 receptors or the central cholinergic system play roles in these cardiovascular effects. Blood pressure and HR were observed before and for 30 min following drug injections. The following results were obtained: 1) icv ADM (750 ng/10 µL) caused an increase in both blood pressure and HR (DMAP = 11.8 ± 2.3 mmHg and ΔHR = 39.7 ± 4.8 bpm). 2) Pretreatment with a CGRP receptor antagonist (CGRP8-37) and ADM receptor antagonist (ADM22-52) blocked the effect of central ADM on blood pressure and HR. 3) The nicotinic receptor antagonist mecamylamine (25 µg/10 µL, icv) and the muscarinic receptor antagonist atropine (5 µg/10 µL, icv) prevented the stimulating effect of ADM on blood pressure. The effect of ADM on HR was blocked only by atropine (5 µg/10 µL, icv). 4) The V1 receptor antagonist [β-mercapto-β-β-cyclopentamethylenepropionyl¹, O-me-Tyr²,Arg8]-vasopressin (V2255; 10 µg/kg), that was applied intravenously, prevented the effect of ADM on blood pressure and HR. This is the first study reporting the role of specific ADM and CGRP receptors, especially the role of nicotinic and muscarinic central cholinergic receptors and the role of peripheral V1 receptors in the increasing effects of icv ADM on blood pressure and HR.

Cardiovascular effects of the intracerebroventricular injection of adrenomedullin: roles of the peripheral vasopressin and central cholinergic systems.

Our objective was to investigate in conscious Sprague-Dawley (6-8 weeks, 250-300 g) female rats (N = 7 in each group) the effects of intracerebroventricularly (icv) injected adrenomedullin (ADM) on blood pressure and heart rate (HR), and to determine if ADM and calcitonin gene-related peptide (CGRP) receptors, peripheral V1 receptors or the central cholinergic system play roles in these cardiovascular effects. Blood pressure and HR were observed before and for 30 min following drug injections. The following results were obtained: 1) icv ADM (750 ng/10 µL) caused an increase in both blood pressure and HR (DMAP = 11.8 ± 2.3 mmHg and ΔHR = 39.7 ± 4.8 bpm). 2) Pretreatment with a CGRP receptor antagonist (CGRP8-37) and ADM receptor antagonist (ADM22-52) blocked the effect of central ADM on blood pressure and HR. 3) The nicotinic receptor antagonist mecamylamine (25 µg/10 µL, icv) and the muscarinic receptor antagonist atropine (5 µg/10 µL, icv) prevented the stimulating effect of ADM on blood pressure. The effect of ADM on HR was blocked only by atropine (5 µg/10 µL, icv). 4) The V1 receptor antagonist [ß-mercapto-ß-ß-cyclopentamethylenepropionyl¹, O-me-Tyr²,Arg8]-vasopressin (V2255; 10 µg/kg), that was applied intravenously, prevented the effect of ADM on blood pressure and HR. This is the first study reporting the role of specific ADM and CGRP receptors, especially the role of nicotinic and muscarinic central cholinergic receptors and the role of peripheral V1 receptors in the increasing effects of icv ADM on blood pressure and HR.

Oxitocina, vasopresina y conducta social: hipótesis neuropéptida para el trastorno autista / Oxytocin, vasopressin and social behavior: neuropeptide hypothesis

Introducción: El Trastorno Autista es una patología de inicio temprano que evoluciona hacia la cronicidad y se caracteriza principalmente por un desarrollo marcadamente anormal o deficiente de la interacción y comunicación social. Es más frecuente en hombres y si bien se presume que es de origen multifactorial, se plantea que puede ser explicado, al menos en parte, por una alteración en la neurobiología que da sustento a las conductas sociales normales. La Oxitocina y la Vasopresina han sido ampliamente relacionadas con las conductas sociales tanto en animales como en humanos, específicamente han sido relacionadas con las conductas de apego, de filiación y con el Trastorno Autista. Objetivos: Entregar un marco teórico que contribuya a organizar el amplio conocimiento que existe sobre la fisiopatología del Trastorno Autista y que entregue luces tanto para la investigación como para la clínica. Método: Se realiza una revisión bibliográfica sobre el rol que juegan la Oxitocina y la Vasopresina en las conductas sociales sanas y anormales tanto en animales como en humanos centrándose la discusión en la relación que tienen estos neuropéptidos con el Trastorno Autista. Conclusiones: Si bien se presume que la fisiopatología del Trastorno Autista es de origen multifactorial, se logra organizar un marco teórico para la comprensión de la fisiopatología del trastorno desde una hipótesis neuropéptida, lo cual tiene implicancias tanto para la investigación como para la clínica.

Introduction: Autistic disorder is an early onset disease that evolves into chronicity, characterized by the presence of markedly abnormal or deficient development of social interaction and communication. It is more common in men and although presumed to be of multifactorial origin, it is proposed that it can be explained, at least in part, by alterations in the neurobiology which gives supports to normal social behavior. Oxytocin and vasopressin have been widely associated with social behavior in animals and humans, specifically with attachment behaviors, affiliation and Autistic Disorder. Objectives: To provide a theoretical framework in order to help organize the extensive knowledge that exists about the pathophysiology of autistic disorder and to deliver light for both research and clinic. Methods: We performed a systematic review of the role played by oxytocin and vasopressin in healthy and abnormal social behavior in both animals and humans and focused the discussion on the relationship that have these neuropeptides with Autistic Disorder. Conclusions: Understanding the pathophysiology of the Autistic Disorder from a neuropeptide hypothesis, provides a theorethical framework which has implications for both research and clinic.

The nanopeptide hormone vasopressin is a new player in the modulation of renal Na(+)-Cl(-) cotransporter activity.

Vasopressin is a modulator of salt and water reabsorption, with known effects in the thick ascending limb and the collecting duct. Pedersen et al. present evidence that vasopressin administration increases the phosphorylation of the apical thiazide-sensitive Na(+)-Cl(-) cotransporter in the distal convoluted tubule. These effects appear to be independent of the renin-angiotensin system and to be mediated by the intracellular kinase SPAK. These observations expand the vasopressin-sensitive region of the nephron.

Oxytocin, but not vassopressin, modulates nociceptive responses in dorsal horn neurons.

Oxytocin (OT) and vasopressin (VP) are synthesized and secreted by the paraventricular hypothalamic nucleus (PVN), and both peptides have been implicated in the pain modulatory system. In the spinal cord, activation of OT-containing axons modulates nociceptive neuronal responses in dorsal horn neurons; however, it is not known whether the direct VPergic descending projection participates. Here, we show that both PVN electrical stimulation and topical application of OT in the vicinity of identified and recorded dorsal horn WDR selectively inhibit Adelta and C-fiber responses. In contrast, the topical administration of VP on the same neurons did not affect the nociceptive responses. In addition, the reduction in nociceptive responses caused by PVN stimulation or OT administration was blocked with a selective OT antagonist. The results suggest that the VP descending projection does not modulate the antinociceptive effects mediated by the PVN on dorsal horn neurons; instead, it is the hypothalamic-spinal OT projection that regulates nociceptive information.

Differential regulation of H+-ATPases in MDCK-C11 cells by aldosterone and vasopressin.

The objective of the present work was to characterize the biochemical activity of the proton pumps present in the C11 clone of Madin-Darby canine kidney (MDCK) cells, akin to intercalated cells of the collecting duct, as well as to study their regulation by hormones like aldosterone and vasopressin. MDCK-C11 cells from passages 78 to 86 were utilized. The reaction to determine H+-ATPase activity was started by addition of cell homogenates to tubes contained the assay medium. The inorganic phosphate (P(i)) released was determined by a colorimetric method modified from that described by Fiske and Subbarow. Changes in intracellular calcium concentration in the cells was determined using the Ca2+-sensing dye fluo-4 AM. Homogenates of MDCK-C11 cells present a bafilomycin-sensitive activity (vacuolar H+-ATPase), and a vanadate-sensitive activity (H+/K+-ATPase). The bafilomycin-sensitive activity showed a pH optimum of 6.12. ATPase activity was also stimulated in a dose-dependent fashion as K+ concentration was increased between 0 and 50 mmol x L(-1), with an apparent K(m) for the release of P(i) of 0.13 mmol x L(-1) and Vmax of 22.01 nmol x mg(-1) x min(-1). Incubation of cell monolayers with 10(-8) mol x L(-1) aldosterone for 24 h significantly increased vacuolar H+-ATPase activity, an effect prevented by 10(-5) mol x L(-1) spironolactone. Vacuolar H+-ATPase activity was also stimulated by 10(-11) mol x L(-1) vasopressin, an effect prevented by a V1 receptor-specific antagonist. This dose of vasopressin determined a sustained rise of cytosolic ionized calcium. We conclude that (i) homogenates of MDCK-C11 cells present a bafilomycin-sensitive (H+-ATPase) activity and a vanadate-sensitive (H+/K+-ATPase) activity, and (ii) vacuolar H+-ATPase activity is activated by aldosterone through a genomic pathway and by vasopressin through V1 receptors.

Vasopressin mediates the pressor effect of hypertonic saline solution in endotoxic shock.

The administration of lipopolysaccharide (LPS) to experimental animals results in a septic shock-like syndrome characterized by hypotension, and the hemodynamic management includes the restoration of adequate tissue perfusion by administration of resuscitation fluids to achieve an effective circulating volume. In the present study, we sought to investigate the effects of hypertonic saline solution administration on vasopressin secretion and mean arterial pressure in endotoxic shock. The pressor response to isotonic saline solution (0.9% sodium chloride) or hypertonic saline (7.5% sodium chloride, 4 mL/kg i.v.) was evaluated 4 h after LPS (1.5 mg/kg) administration. At this moment, plasma vasopressin did not differ from control; however, the blood pressure was lower in the LPS-treated group. The hypertonic saline administration was followed by an immediate recovery of blood pressure and also by an increase in plasma vasopressin levels compared with isotonic saline solution. The vasopressin V1 receptor antagonist (10 microg/kg, i.v., 5 min before infusion) blocked the pressor response to hypertonic saline solution. These data suggest that the recovery of blood pressure after hypertonic saline solution administration during endotoxic shock is mediated by vasopressin secretion.

Pressor response to chemoreflex activation in awake rats: role of vasopressin and adrenal medulla.

The possible role of the peptide vasopressin and adrenal catecholamine in the pressor response to chemoreflex activation was evaluated in awake rats. Data show that the peripheral blockade of the V1 vasopressin receptor produced no change in the cardiovascular responses to chemoreflex activation, indicating that vasopressin plays no role on the pressor response to chemoreflex activation. We also have shown that the pressor response to chemoreflex activation is dependent on the sympathetic efferent activity since the antagonism of the alpha1-adrenoceptor with prazosin almost abolished the pressor response to chemoreflex activation. Furthermore, bilateral adrenal demedullation produced no change on the pressor response to chemoreflex activation, outpointing that the release of catecholamines by the adrenal medulla is not involved in the pressor response to chemoreflex. We conclude that the pressor response to chemoreflex activation is essentially mediated by the sympathetic innervations to the peripheral vascular beds.

Involvement of prolactin, vasopressin and opioids in post-ictal antinociception induced by electroshock in rats.

The neurochemical mechanisms involved in post-ictal antinociception remain to be elucidated. Application of electroconvulsive shock (ECS) to rats results in post-ictal antinociception. The objective of this study was to identify endogenous substances that could participate in antinociception during post-ictal depression induced by ECS (70 mA, 60 Hz, 1 s). Antinociception was measured by the rat paw-pressure test, in which increased sensitivity is induced by intraplantar injection of carrageenan. This test proved to be efficient in detecting the electroshock-induced antinociception. Intense post-ictal antinociception was observed over a period of 30 min after the end of the seizure. It was used nonspecific opioid and specific vasopressin antagonists and the prolactin (PRL) release inhibitor to test the reversal of antinociception. Administration of naloxone (5, 7.5 and 10 mg/kg) blocked the post-ictal antinociception. The V(1) (125 microg/kg) and V(2) (250 microg/kg) vasopressin receptor antagonists ([beta-mercapto-beta,beta-cyclopentamethylenepropionyl(1),O-Et-Tyr(2),Val(4),Arg(8)]-vasopressin and [adamantaneacetyl(1),O-Et-d-Tyr(2),Val(4),Abu(6),Arg(8,9)]-vasopressin) also inhibited the nociceptive response. The antinociception blockade was more intense after administration of the V(1) receptor antagonist. Bromocriptine (4, 8 and 12 mg/kg) was able to reverse antinociception behavior during the post-ictal period. Morphine (1, 2 and 4 mg/kg), vasopressin (12.5, 100 and 400 microg/kg) and prolactin (100, 200 and 400 microg/kg) administration promoted a higher nociceptive threshold. It was administered the three substances with their respective antagonists to verify the opioidergic pathway and vasopressin and prolactin release interactions, and as a positive control. We observed that the tested mediators were released in an independent manner, indicating no interference in which other.

[Vasopressin use in shock]. / Uso de la vasopresina en el estado de choque.

Arginine-vasopressin (VP), also known as the antidiuretic hormone, is essential for water homeostasis. Its synthesis and liberation depends on regulation of osmotic, hypovolemic, hormonal, and nonosmotic stimuli. It has been demonstrated that it is key for maintenance of cardiovascular homeostasis through vasomotor regulation, the determinant of systemic vascular resistance and mean arterial pressure, a process acting through V1 receptors. Shock state with refractory vasodilation seen in sepsis, systemic inflammatory response, hypovolemia, cardiac arrest, polytrauma, etc., is characterized by an initial phase of liberation and increased levels of VP followed by a second phase characterized by inappropriately low levels of this hormone that are associated with refractoriness to management with volume, inotropics, and vasopressors. It has been demonstrated in clinical and experimental studies that exogenous VP treatment under this condition increases systemic vascular resistance, perfusion pressure, and oxygen supply to peripheral tissues, which makes it possible to decrease and to suspend vasopressors and also to increase survival.

Uso de la vasopresina en el estado de choque / Vasopressin Use in Shock

La arginina-vasopresina (VP) también conocida como hormona antidiurética es esencial para mantener el equilibrio hídrico. Su síntesis y liberación depende de la interacción de estímulos osmóticos, hipovolémicos, hormonales y no osmóticos. Se ha demostrado que en estados de choque es fundamental para mantener la homeostasis cardiovascular a través de la regulación del tono vasomotor, el cual determina las resistencias vasculares sistémicas y la presión arterial media, a través de los receptores VI. El estado de choque con vasodilatación refractaria que se presenta en sepsis, respuesta inflamatoria sistémica, hipovolemia, paro cardiaco, politraumatismo, etc... se caracteriza por una fase inicial en la que hay liberación y aumento en los niveles séricos de VP, ésta es seguida por una segunda fase en la que se presentan niveles inapropiadamente bajos de la hormona y éstos se asocian con refractariedad al manejo con volumen, inotrópicos y vasopresores. Se ha demostrado, en estudios experimentales y clínicos, que en esta condición el tratamiento con vasopresina exógena incrementa la resistencia vascular sistémica, la presión de perfusión y el aporte de oxígeno a los tejidos periféricos lo cual hace posible la disminución y suspensión de los vasopresores e incrementa la supervivencia.

Arginine-vasopresin (VP), also known as the antidiuretic hormone, is essential for water homeostasis. Its synthesis and liberation depends on regulation of osmotic, hypovolemic, hormonal, and nonosmotic stimuli. It has been demonstrated that it is key for maintenance of cardiovascular homeostasis through vasomotor regulation, the determinant of systemic vascular resistance and mean arterial pressure, a process acting through VI receptors. Shock state with refractary vasodilation seen in sepsis, systemic inflamatory response, hypovolemia, cardiac arrest, polytrauma, etc., is characterized by an initial phase of liberation and increased levels of VP followed by a second phase caracterized by inappropirately low levels of this hormone that are associated with refractariness to management with volume, inotropics, and vasopressors. It has been demonstrated in clinical and experimental studies that exogenous VP treatment under this condition increases systemic vascular resistance, perfusion pressure, and oxygen supply to peripheral tissues, which makes it possible to decrease and to suspend vasopressors and also to increase survival.

Neuroendocrine control of body fluid metabolism.

Mammals control the volume and osmolality of their body fluids from stimuli that arise from both the intracellular and extracellular fluid compartments. These stimuli are sensed by two kinds of receptors: osmoreceptor-Na+ receptors and volume or pressure receptors. This information is conveyed to specific areas of the central nervous system responsible for an integrated response, which depends on the integrity of the anteroventral region of the third ventricle, e.g., organum vasculosum of the lamina terminalis, median preoptic nucleus, and subfornical organ. The hypothalamo-neurohypophysial system plays a fundamental role in the maintenance of body fluid homeostasis by secreting vasopressin and oxytocin in response to osmotic and nonosmotic stimuli. Since the discovery of the atrial natriuretic peptide (ANP), a large number of publications have demonstrated that this peptide provides a potent defense mechanism against volume overload in mammals, including humans. ANP is mostly localized in the heart, but ANP and its receptor are also found in hypothalamic and brain stem areas involved in body fluid volume and blood pressure regulation. Blood volume expansion acts not only directly on the heart, by stretch of atrial myocytes to increase the release of ANP, but also on the brain ANPergic neurons through afferent inputs from baroreceptors. Angiotensin II also plays an important role in the regulation of body fluids, being a potent inducer of thirst and, in general, antagonizes the actions of ANP. This review emphasizes the role played by brain ANP and its interaction with neurohypophysial hormones in the control of body fluid homeostasis.

[Vasopressin: uses in cardiovascular practice]. / Vasopresina: usos en la práctica cardiovascular.

Vasopressin is secreted by the neurohypophysis influenced by many variables; among them the most important and known is the osmotic pressure (osmotic regulation) of body fluid. Other factors that modify this hormone's secretion are changes in blood volume and blood pressure, which contribute significantly to hemodynamic recovery. Vasopressin receptors are located in different sites, and their stimulation generate also generates different physiological responses. The receptors are of two types, V1 and V2. The usefulness of exogenous vasopressin has been proven in many clinical situations, refractory cardiac arrest, septic shock, vasodilator shock, postcardiotomy shock, and vasoplegic shock, with promising results. At present, enough scientific support exists for the use of this antidiuretic hormone (vasopressin) in clinical practice.

Role of vasopressin in 24-hour blood pressure regulation in diabetic patients with autonomic neuropathy.

To evaluate the role of vasopressin (AVP) on blood pressure (BP) in diabetic patients with autonomic neuropathy (AN), 10 patients were studied on a fixed sodium and potassium diet. On days 4 and 7, a 24-h BP monitoring, as well as blood and urine samples for sodium, potassium, creatinine, and osmolality determinations were obtained for every 4-h period; either placebo or an AVP-V1-antagonist (d(CH2)5Tyr(me)AVP; 0.5 mg; AVPi) were given iv at 1 PM. On placebo, systolic BP (SBP) showed a progressive elevation during the day, declining after 12 PM (8 AM to 12 AM 122+/-9; 12 AM to 4 PM 125+/-11; 4 PM to 8 PM 134+/-14; 8 PM to 12 PM 136+/-14; 12 PM to 8 AM 131+/-17 mm Hg). On AVPi this rise in SBP was blunted: 8 AM to 12 AM 125+/-122; 12 AM to 4 PM 121+/-21; 4 PM to 8 PM 126+/-16; 8 PM to 12 PM 129+/-14; 12 PM to 8 AM 124+/-12 mm Hg. Creatinine clearance and diureses were greater during the night, both with placebo and AVPi. Plasma osmolality did not change on either day, although serum sodium decreased after AVPi, reaching the lowest values at 4 PM to 8 PM period (137+/-4.7 v 131+/-3.8 mEq/L; P < .05). With placebo, fractional excretion of sodium (FENa) increased from 0.43%+/-0.32% during 12 h of orthostasis to 0.92%+/-1.05% during 12 h of recumbency (P < .02). With AVPi, the FENa on orthostasis did not differ from that with placebo, although BP values were lower and did not increase with recumbency (0.58+/-0.57 v 0.73%+/-0.49%; NS). In conclusion, our results show that in diabetic patients with AN, vasopressin participates in BP control by stimulating vascular and renal V1 receptors, which results in vasoconstriction and sodium reabsorption.