Effect of Plasma Osmolality on Pituitary-Adrenal Responses to Corticotropin-Releasing Hormone and Atrial Natriuretic Peptide Changes in Central Diabetes Insipidus

Elias, L. L. K.

doi:10.1210/jc.82.4.1243

Cited by 47 publications

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“…Growth retardation is also observed in patients with nephrogenic DI (14,23). Several factors could predispose patients with untreated DI to growth failure, such as decreased calorie intake due to predominant fluid consumption or loss of appetite because of an activated hypothalamic-pituitary axis (HPA) stress axis in chronic hyperosmolality (24). Upon treatment of the AVP deficiency by DDAVP, a catch-up growth over several months occurred in all our patients.…”

Section: Discussionmentioning

confidence: 82%

Growth retardation in untreated autosomal dominant familial neurohypophyseal diabetes insipidus caused by one recurring and two novel mutations in the vasopressin-neurophysin II gene

Brachet

Birk

Christophe

et al. 2011

European Journal of Endocrinology

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Objective: Autosomal dominant familial neurohypophyseal diabetes insipidus (adFNDI), a disorder caused by mutations in the vasopressin (AVP)-neurophysin II (NPII) gene, manifests gradually during early childhood with progressive polyuria and polydipsia. Patients are usually treated with synthetic AVP analog. If unlimited access to water is provided, prognosis is usually good even in the absence of specific treatment.In this study, we describe three families with adFNDI, in which growth failure was a prominent complaint, on the clinical and molecular level. Design/methods: Histories from affected and unaffected family members were taken. Height and weight of index patients were recorded longitudinally. Patients underwent water deprivation tests, magnetic resonance imaging, and genetic analysis. One mutant was studied by heterologous expression in cell culture. Results: A total of ten affected individuals were studied. In two of the three pedigrees, a novel mutation in the AVP-NPII gene was found. The index children in each pedigree showed growth retardation, which was the reason for referral in two. In these cases, water intake was tightly restricted by the parents in an attempt to overcome suspected psychogenic polydipsia and to improve appetite. Once the children were treated by hormone replacement, they rapidly caught up to normal weight and height. Conclusions: Genetic testing and appropriate parent counseling should be enforced in adFNDI families to ensure adequate treatment and avoid chronic water deprivation, which causes failure to thrive.

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Section: Discussionmentioning

confidence: 82%

Growth retardation in untreated autosomal dominant familial neurohypophyseal diabetes insipidus caused by one recurring and two novel mutations in the vasopressin-neurophysin II gene

Brachet

Birk

Christophe

et al. 2011

European Journal of Endocrinology

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“…Plasma levels of ANP, OT, and VP were measured by radioimmunoassay as previously described (16,23,24). VP and OT were extracted from 1 ml of plasma with acetone and petroleum ether, and ANP was extracted from 1 ml of plasma using Sep-Pak C-18 cartridges (Waters, Milford, MA).…”

Section: Determination Of Plasma Anp Ot and Vp Concentrationsmentioning

confidence: 99%

Serotonergic mechanisms of the lateral parabrachial nucleus in renal and hormonal responses to isotonic blood volume expansion

Margatho

Giusti‐Paiva²,

Menani³

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

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This study investigated the involvement of serotonergic mechanisms of the lateral parabrachial nucleus (LPBN) in the control of sodium (Na ϩ ) excretion, potassium (K ϩ ) excretion, and urinary volume in unanesthetized rats subjected to acute isotonic blood volume expansion (0.15 M NaCl, 2 ml/100 g of body wt over 1 min) or control rats. Plasma oxytocin (OT), vasopressin (VP), and atrial natriuretic peptide (ANP) levels were also determined in the same protocol. Male Wistar rats with stainless steel cannulas implanted bilaterally into the LPBN were used. In rats treated with vehicle in the LPBN, blood volume expansion increased urinary volume, Na ϩ and K ϩ excretion, and also plasma ANP and OT. Bilateral injections of serotonergic receptor antagonist methysergide (1 or 4 g/200 l) into the LPBN reduced the effects of blood volume expansion on increased Na ϩ and K ϩ excretion and urinary volume, while LPBN injections of serotonergic 5-HT2a/HT2c receptor agonist, 2.5-dimetoxi-4-iodoamphetamine hydrobromide (DOI; 1 or 5 g/200 l) enhanced the effects of blood volume expansion on Na ϩ and K ϩ excretion and urinary volume. Methysergide (4 g) into the LPBN decreased the effects of blood volume expansion on plasma ANP and OT, while DOI (5 g) increased them. The present results suggest the involvement of LPBN serotonergic mechanisms in the regulation of urinary sodium, potassium and water excretion, and hormonal responses to acute isotonic blood volume expansion. serotonin; natriuresis; atrial natriuretic peptide; oxytocin; vasopressin ISOTONIC BLOOD VOLUME expansion, by reflex mechanisms, induces a series of regulatory responses, including the inhibition of the sympathetic outflow to the kidney, heart, and blood vessels, reduction of renin and vasopressin (VP) secretion, and increase in the levels of circulating atrial natriuretic peptide (ANP) and oxytocin (OT) that leads to diuresis and natriuresis (1,2,12,14,20,24,45,53).There are several reports demonstrating the correlation between natriuresis and diuresis and plasma ANP levels in response to systemic volume expansion, e.g., atrial balloon inflation, blood volume expansion, salt load, and water immersion (4,7,17,32,50,59). These responses depend on the activation of sinoaortic baroreceptors and/or cardiopulmonary receptor afferents located in the atria, lungs, great veins, and ventricles that project to the nucleus of the solitary tract (NTS) (1, 12, 22). The NTS neurons convey blood volume expansion signals and project to and excite different areas within the forebrain and hindbrain to produce neuroendocrine responses. Studies using expression of the immediate early gene c-Fos as a marker of neuronal activation have shown that, in addition to the NTS, volume-loading activates the paraventricular (PVN) and supraoptic (SON) nuclei, dorsal raphe nucleus (DRN), caudal ventrolateral medulla, locus coeruleus, and also the lateral parabrachial nucleus (LPBN) (6,20,46). The LPBN, a structure lying dorsolateral to the superior cerebellar peduncle, has been shown to play an ...

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“…AVP concentration was measured by radioimmunoassay (RIA) after extraction of plasma (1 mL) with acetone and petroleum ether, at the Laboratory of Endocrine Physiology, Ribeirão Preto School of Medicine, University of São Paulo, as previously reported [18]. The percentage of recovery after extraction was 83% (ranging from 50% to 99%).…”

Section: Methods For Hormonal Determinationmentioning

confidence: 99%

Vasopressina plasmática em pacientes submetidos à correção de aneurisma de aorta infrarrenal

Carvalho¹,

Guillaumon²,

Cintra³

et al. 2011

Rev Bras Cir Cardiovasc

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Objectives: To evaluate plasmatic arginine vasopressin (AVP) levels in patients undergoing scheduled conventional abdominal aortic aneurysm (AAA) repair.Methods: Plasmatic AVP concentrations were measured by radioimmunoassay in 22 non-consecutive adult patients undergoing infra-renal AAA repair. They were under combined general and epidural anesthesia at the following time frames: 1 -pre-operative (T0); 2 -2h (T1) and 6h (T2) after the surgical procedure; 3 -in the morning at the first (T3), second (T4) and third (T5) post-operative days. Some clinical and laboratory variables were also recorded.Results: The mean age of patients was 68±10 years; 17 were males. Plasmatic AVP (mean±SD; pg/mL) was within the normal range at T0 (1.4±0.7; baseline), increasing significantly at T1 (62.6±62.9; P<0.001) and at T2 (31.5±49.7; P<0.001), with a progressive fall, returning to basal levels at T5 (2.1±3.8; P=NS). Positive and statistically significant correlations were found between AVP and glycemia, serum lactate and white blood cells counts, but not with systemic arterial pressure or plasma osmolarity during the postoperative period.Conclusions: Considering that no correlations were found between AVP levels and hemodynamic or plasmatic osmolarity variations in AAA repair, it seems that stress response is mainly secondary to noxious stimulation mediated by the autonomic nervous system that is not completely blocked by anesthetics. Descriptors: Intensive care units. Cardiovascular abnormalities. Receptors, vasopressin. Resumo Objetivos: Avaliar os níveis plasmáticos de vasopressina (AVP) em pacientes submetidos à correção convencional de aneurisma de aorta abdominal (AAA).Métodos: A AVP plasmática foi mensurada por radioimunoensaio em 22 pacientes não-consecutivos submetidos à correção eletiva de AAA infrarrenal sob anestesia geral + epidural nos seguintes momentos: pré-operatório (T0); 2h (T1) e 6h (T2) após a cirurgia; e nas manhãs do primeiro (T3), segundo (T4) e terceiro (T5) dia pós-operatório (PO). Variáveis clínicas e laboratoriais de interesse também foram anotadas.Resultados: A média de idade dos pacientes foi de 68±10 anos, sendo 17 homens. A AVP plasmática (média±DP; pg/ mL) estava dentro de limites normais no T0 (1,4±0,7; basal), aumentando no T1 (62,6±62,9; P<0,001) e no T2 (31,5±49,7; P<0,001), e retornando aos valores basais no T5 (2,1±3,8; RBCCV 44205-1296

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Effect of Plasma Osmolality on Pituitary-Adrenal Responses to Corticotropin-Releasing Hormone and Atrial Natriuretic Peptide Changes in Central Diabetes Insipidus

Cited by 47 publications

References 0 publications

Growth retardation in untreated autosomal dominant familial neurohypophyseal diabetes insipidus caused by one recurring and two novel mutations in the vasopressin-neurophysin II gene

Growth retardation in untreated autosomal dominant familial neurohypophyseal diabetes insipidus caused by one recurring and two novel mutations in the vasopressin-neurophysin II gene

Serotonergic mechanisms of the lateral parabrachial nucleus in renal and hormonal responses to isotonic blood volume expansion

Vasopressina plasmática em pacientes submetidos à correção de aneurisma de aorta infrarrenal

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