Plasma Vasopressin Levels Research Articles

Disorders of Water and Sodium Balance

Water accounts for approximately half of an adult human’s body weight. Two thirds of body water is intracellular, and the remaining one third is contained in the extracellular fluid compartment, which includes intravascular (plasma) and interstitial fluid. Small amounts of water are also contained in bone, dense connective tissue, digestive secretions, and cerebrospinal fluid. To maintain the stability of the internal milieu, body fluids are processed by the kidney, guided by intricate physiologic control systems that regulate fluid volume and composition. This chapter reviews the regulation of body fluid volumes, cell volume regulation in hypotonicity and hypertonicity, disorders of water excess (hyponatremia), water deficiency (hypernatremia), water conservation (diabetes insipidus), saltwater excess (edematous states), and saltwater deficiency (volume depletion). Tables describe control of body fluid volumes, causes of nonhypotonic hyponatremia, causes and treatment of acute hyponatremia, causes of the syndrome of inappropriate release of antidiuretic hormone (SIADH), and causes of hypernatremia. Figures illustrate sodium reabsorption by the renal tubules, the relationship between plasma vasopressin levels, renal sodium handling, and dose-response curves for a loop diuretic in patients with normal and reduced renal function. This chapter contains 4 highly rendered figures, 5 tables, 88 references, and 5 MCQs.

Serious Adverse Events Associated With Vasopressin and Norepinephrine Infusion in Septic Shock*

The frequency, risk factors, and mortality rates of serious adverse events associated with the use of vasopressin and norepinephrine are not clear. The objectives of this study were to determine frequency, risk factors (including candidate gene polymorphisms), and outcomes of serious adverse events in septic shock patients. Retrospective cohort study using multicenter discovery and single-center validation cohorts. ICUs at academic teaching centers. Five hundred ninety-seven patients with septic shock in discovery (Vasopressin and Septic Shock trial) and 533 patients in validation (St. Paul's Hospital) cohorts. Vasopressin and norepinephrine for septic shock. The primary outcome variable was 90-day mortality rates of patients with and without serious adverse events. Secondary outcome variables were the association between vasopressor genotype pathway polymorphisms, plasma vasopressin levels, and serious adverse events. Plasma vasopressin concentrations were measured at baseline, 6 hours, 24 hours, 72 hours, and 7 days after vasopressor infusion. Patients with septic shock were genotyped for 268 vasopressor pathway tag single-nucleotide polymorphisms. Serious adverse events occurred in 10.5% and 9.7% of patients in Vasopressin and Septic Shock trial and St. Paul's Hospital cohorts, respectively. Patients who had serious adverse events had higher mortality (p < 0.01) than patients without serious adverse events (adjusted for age, serum lactate, Acute Physiology and Chronic Health Evaluation II, and maximum dose of norepinephrine day 1) (hazard ratio, 2.97; 95% CI, 2.20-4.00; p < 0.001 and hazard ratio, 1.89; 95% CI, 1.26-2.85; p = 0.002 in Vasopressin and Septic Shock trial and St. Paul's Hospital, respectively). There was no difference in the area under the plasma vasopressin concentration curve between patients with and without serious adverse events (p = 0.1). The AA genotype of rs28418396 single-nucleotide polymorphism (near the arginine vasopressin receptor 1b gene) was significantly associated with serious adverse events in discovery and validation cohorts (p = 0.001 and p = 0.04, respectively). Serious adverse events associated with vasopressin and norepinephrine in patients who have septic shock are associated with increased mortality and morbidity. AA genotype of rs28418396 single-nucleotide polymorphism near the arginine vasopressin receptor 1b gene is associated with serious adverse events. The mechanism of this association requires investigation.

Urinary concentration does not exclusively rely on plasma vasopressin. A study between genders. Gender and diurnal urine regulation.

We investigated the influence of gender on the diurnal regulation of urine production with special focus on vasopressin, oxytocin and prostaglandin E2. Fifteen young women in mid-follicular phase and 22 young men (20-33years) were included. All participants underwent a 24-h circadian inpatient study under standardized conditions for measurements of plasma vasopressin, oxytocin, sodium and osmolality. Urine was fractionally collected for measurements of electrolytes, aquaporin-2 and prostaglandin E2. Plasma vasopressin expressed a diurnal rhythm with a night-time increase in both genders (P<0.001). The ratio between mean daytime and mean night-time was 1.57 [95% CI: 1.33-1.84] P<0.001 in men and 1.35 [95% CI: 1.11-1.64] P=0.002 in women. P-vasopressin was higher in males during the night (P<0.05). There was no difference in diuresis (P=0.43), urine osmolality (P=0.12) or aquaporin-2 excretion (P=0.80) between genders. We found a trend towards a higher reabsorption of free water in males (P=0.07). The excretion of prostaglandin E2 was higher in males (P<0.001). There was no diurnal rhythm in p-oxytocin (P=0.37) and no correlation to diuresis, urine osmolality or aquaporin-2 excretions. Similar urinary flows and osmolalities are associated with levels of plasma vasopressin and renal PGE2, which are higher in males than in females. Oxytocin does not seem to play a role in the diurnal urine formation, whereas prostaglandin E2 could represent a mediator of the gender difference, not only as a mediator of the vasopressin response, but also as an independent factor. These findings need further elucidation.

Development and validation of a highly sensitive LC–MS/MS assay for the quantification of arginine vasopressin in human plasma and urine: Application in preterm neonates and child

Arginine vasopressin is an endogenous neuropeptide secreted in response to situations such as hyperosmolality, hypotension and hypovolemia. The purpose of this study was to develop a reliable assay using small volumes of plasma and urine samples to quantify vasopressin levels in preterm infants. Weak cation solid-phase extraction was used to extract vasopressin from 200μl human plasma and urine samples. Separation was achieved on a Waters Acquity UPLC BEH C18 column by gradient elution at 0.55ml/min, with a mobile phase composed of methanol and 0.02% aqueous acetic acid solution. Analysis was performed under a hybrid triple quadrupole linear ion trap mass spectrometer, operated in multiple reaction monitoring mode using positive ionization. The linear response range was 1.0–40pg/ml for vasopressin, with the lower limit of quantification (LLOQ) of 1.0pg/ml in human plasma and urine. Recoveries at concentrations of 3, 10 and 32pg/ml were all greater than 70%, and matrix effects were within 15%. The method was validated with intra-day and inter-day precision of less than 8% for human plasma and urine. The intra-day and inter-day accuracy for human plasma were 91.9–100.6% and 92.3–104.8%, respectively. The intra-day and inter-day accuracy for human urine were 89.2–95.9% and 89.3–91.3%, respectively. The validated method was successfully applied to analyze two preterm neonate plasma samples and one child urine sample. In conclusion, the developed and validated method was sensitive and reliable, and was successfully used to quantify endogenous vasopressin levels in neonate plasma and child urine.

Gastric dysrhythmias: a potential objective measure of nausea

Nausea is a noxious, uncomfortable feeling usually located in the epigastrium. The pathophysiology of nausea encompasses brain-gut and gut-brain interaction. Nausea is associated with myoelectrical dysrhythmias of the stomach, an objective marker in the periphery. The aims of this review were to describe (1) the physiology of normal 3cycle per minute (cpm) gastric myoelectrical activity and (2) conditions where shifts from normal 3cpm gastric rhythms to gastric dysrhythmias are associated with the onset of nausea. Illusory self-motion, infusion of drugs such as morphine and glucagon, and ingestion of water or nutrient loads are several of the multitude of stimuli that induce acute nausea and a variety of gastric dysrhythmias such as tachygastrias (3.75-10cpm) and bradygastrias (1.0-2.5cpm). In nausea of motion sickness, increased nausea severity correlates with increased plasma vasopressin and epinephrine levels. Gastric dysrhythmias are also present in chronic gastrointestinal neuromuscular disorders such as gastroparesis. When gastric dysrhythmias resolve after drug or device therapies, nausea resolves. The shift in state from comfort in the epigastrium area and normal 3cpm gastric rhythm to symptoms of nausea and gastric dysrhythmias represents dynamic gut-brain and brain-gut interactions that can be tracked by changes in gastric rhythm. (1) gastric dysrhythmias represent at least one peripheral mechanism underlying the symptom of nausea, and (2) gastric dysrhythmias are an objective biomarker for nausea and potential therapeutic targets for anti-nauseant therapies.

The Interaction of Vasopressin and Corticosteroids in Septic Shock

Vasopressin and corticosteroids are both commonly used adjunctive therapies in septic shock. Retrospective analyses have suggested that there may be an interaction between these drugs, with higher circulating vasopressin levels and improved outcomes in patients treated with both vasopressin and corticosteroids. We aimed to test for an interaction between vasopressin and corticosteroids in septic shock. Prospective open-label randomized controlled pilot trial. Four adult ICUs in London teaching hospitals. Sixty-one adult patients who had septic shock. Initial vasopressin IV infusion titrated up to 0.06 U/min and then IV hydrocortisone (50 mg 6 hourly) or placebo. Plasma vasopressin levels were measured at 6-12 and 24-36 hours after hydrocortisone/placebo administration. Thirty-one patients were allocated to vasopressin + hydrocortisone and 30 patients to vasopressin + placebo. The hydrocortisone group required a shorter duration of vasopressin therapy (3.1 d; 95% CI, 1.1-5.1; shorter in hydrocortisone group) and required a lower total dose of vasopressin (ratio, 0.47; 95% CI, 0.32-0.71) compared with the placebo group. Plasma vasopressin levels were not higher in the hydrocortisone group compared with the placebo group (64 pmol/L difference at 6- to 12-hour time point; 95% CI, -32 to 160 pmol/L). Early vasopressin use was well tolerated with only one serious adverse event possibly related to study drug administration reported. There were no differences in mortality rates (23% 28-day mortality in both groups) or organ failure assessments between the two treatment groups. Hydrocortisone spared vasopressin requirements, reduced duration, and reduced dose, when used together in the treatment of septic shock, but it did not alter plasma vasopressin levels. Further trials are needed to assess the clinical effectiveness of vasopressin as the initial vasopressor therapy with or without corticosteroids.

Changes of atrial natriuretic peptide and antidiuretic hormone in children with postural tachycardia syndrome and orthostatic hypertension: a case control study

Background The abnormal blood volume regulation is one of the most important pathogenesis in postural tachycardia syndrome in children. This study was designed to investigate the plasma atrial natriuretic peptide and antidiuretic hormone levels in postural tachycardia syndrome children, and their associations with the changes in heart rate and blood pressure in head-up test. Methods Twenty-one postural tachycardia syndrome patients ((12±2) years) and 26 healthy children ((12±1) years) were included. According to blood pressure changes in head-up test, the postural tachycardia syndrome patients were divided into two subgroups: postural tachycardia syndrome with orthostatic hypertension and postural tachycardia syndrome without orthostatic hypertension. The plasma atrial natriuretic peptide and antidiuretic hormone levels were measured using enzyme-linked immunosorbent assay. Results The plasma atrial natriuretic peptide level in postural tachycardia syndrome patients was higher than the control (P=0.004), whereas the difference in plasma antidiuretic hormone level between postural tachycardia syndrome and controls was not significant (P=0.222). The plasma antidiuretic hormone level of patients suffering from postural tachycardia syndrome with orthostatic hypertension was much higher than that of children having postural tachycardia syndrome without orthostatic hypertension (P &lt;0.05). In postural tachycardia syndrome patients, the upright max heart rate was positively correlated with the plasma atrial natriuretic peptide level (r=0.490, P&lt;0.05) and the upright systolic blood pressure was positively correlated with the plasma antidiuretic hormone levels (r=0.472, P &lt;0.05). Conclusions There was a disturbance of plasma atrial natriuretic peptide and antidiuretic hormone in postural tachycardia syndrome children. Chin Med J 2014;127 (10): 1853-1857

Arginine vasopressin plasma levels change seasonally in African striped mice but do not differ between alternative reproductive tactics

Arginine vasopressin (AVP) is an important hormone for osmoregulation, while as a neuropeptide in the brain it plays an important role in the regulation of social behaviors. Dry habitats are often the home of obligately sociable species such as meerkats and Damaraland mole-rats, leading to the hypothesis that high plasma AVP levels needed for osmoregulation might be associated with the regulation of social behavior. We tested this in a facultative sociable species, the African striped mouse (Rhabdomys pumilio). During the moist breeding season, both solitary- and group-living reproductive tactics occur in this species, which is obligatory sociable in the dry season. We collected 196 plasma samples from striped mice following different reproductive tactics both during the moist and the dry season. Solitary mice did not have lower AVP levels than sociable mice, rejecting the hypothesis that peripheral AVP is involved in the regulation of alternative reproductive tactics. However, we found significantly higher AVP levels during the dry season, with AVP levels correlated with the abundance of food plants, the main source of water for striped mice. Plasma AVP levels were not correlated with testosterone or corticosterone levels. Our study underlines the important role that AVP plays in osmoregulation, particularly for a free ranging mammal living under harsh arid conditions.

Can vasopressin induce milk ejection in the dairy goat?

Suckling increases plasma levels of both oxytocin (OT) and vasopressin (AVP) and intravenous infusions of AVP increase milk flow and milk fat concentration in goats. We hypothesized that vasopressin can cause contraction of the myoepithelial cells and thereby milk ejection. Eight goats were used in each of two series. They were kept together with their kids and were both suckled and hand milked. At experiments, one teat was first emptied by hand and after 3min the same teat was milked again. On control days, cisternal milk (CM) was achieved at the first milking and at the second milking only a small volume of alveolar milk (AM) with modest fat content was received. On experimental days the goats were milked and immediately thereafter OT (10mg) or AVP at the low dose 125ng (AVPL) was injected intravenously followed by the second milking 3min after the first (series I). In series II saline (0.9% NaCl) or vasopressin at the high dose 250ng (AVPH) was injected. The plasma OT concentrations were unchanged after AVP injections. The CM volume did not differ between treatments within each series. Injections of AVPH or OT increased volume and fat content of AM. The proportion of AM to total milk volume was 15% in control experiments, 21% after saline and 29% after AVPL. However, after AVPH and OT the AM proportions were 56 and 57%, respectively, accompanied by an increased fat content. In conclusion, the high dose of AVP elicited a milk ejection reflex similar to that of OT.

Carotid blood flow, cardiovascular and endocrine responses during head-up tilt in patients with acute cerebrovascular diseases.

The purpose of this study was to define common carotid blood flow (CBF), cardiovascular and endocrine responses during head-up tilt (HUT) in patients with acute cerebrovascular diseases (CVD). In 31 male patients with acute CVD (damage of the supratentorial area) and 21 age-matched control male subjects, we measured CBF, mean blood pressure (MBP), heart rate, stroke volume and cardiac output responses before (baseline), during and after HUT. We also measured plasma levels of antidiuretic hormone, adrenaline, noradrenaline, aldosterone and plasma renin activity. After obtaining baseline measurements during 3-minutes horizontal position, HUT was performed for 5 minutes, followed by continuation of recording for 3 more minutes in the horizontal position. During HUT, CBF decreased significantly and equally in both groups. MBP did not change during HUT in both groups. The endocrine responses were also not different between the two groups. The results suggest that damage to the supratentorial area in patients with acute CVD do not alter the CBF, cardiovascular and endocrine responses. In other words, HUT does not predispose patients with acute CVD to serious falls in MBP and CBF at upright posture.

Plasma vasopressin levels in patients with right-sided heart dysfunction and chronic thromboembolic pulmonary hypertension (CTEPH).

Patients with left-sided heart dysfunction and volume overload often have associated elevations in vasopressin from neuroendocrine activation. The authors investigated perioperative levels of vasopressin in patients with isolated right-sided heart dysfunction from chronic thromboembolic pulmonary hypertension. Prospective, observational study. Single center, tertiary hospital. Patients with chronic thromboembolic pulmonary hypertension undergoing pulmonary thromboendarterectomy. Vasopressin levels were measured in 22 patients during the perioperative period. Vasopressin was undetectable in 8/22 patients at baseline. As a group, vasopressin levels at baseline and after induction of anesthesia were 0.8 pg/mL (median; 0.5-1.5, interquartile range of 25% and 75%) and 0.7 pg/mL (median; 0.5-1.4, interquartile range of 25% and 75%), respectively. During cardiopulmonary bypass (CPB), vasopressin increased to 13.9 pg/mL (median; 6.7-19.9, interquartile range of 25% and 75%). Vasopressin remained elevated after deep hypothermic circulatory arrest (DHCA) at 10.5 pg/mL (median; 6.5-19.9 interquartile range of 25% and 75%) and after CPB at 19.9 pg/mL (median; 11.1-19.9 interquartile range of 25% and 75%). Vasopressin levels in PTE patients are in the low-to-normal range at baseline and may be a clinically relevant issue in the hemodynamic management of PTE.

IMPACTS OF ANTI-DIURETIC HORMONE BY SALT SUPPLEMENTATION IN ACUTE DECOMPENSATED HEART FAILURE

Recent reports have provided findings that severe salt restriction may be harmful in acute decompensated heart failure (ADHF). We have reported that salt supplementation enhances diuretic effects in ADHF. Salt administration generally increases a plasma anti-diuretic hormone (ADH) level. It induces

Autonomous Device for Application in Late-Phase Hemorrhagic Shock Prevention

Hemorrhagic shock (HS) is the leading cause of death for people with traumatic injuries. The onset of HS is correlated with marked changes in the plasma vasopressin levels and some studies indicate that administrating vasopressin in the bloodstream can help stabilize the situation. This situation calls naturally for the use of implantable devices for both the monitoring and treatment of HS. In this work, we present a self-powered hemorrhagic-shock autonomous integrated device (hemoAID) that continuously monitors vasopressin levels and releases vasopressin automatically when levels drop below a certain threshold. We demonstrate that the device can operate at physiological concentrations of vasopressin, in sheep serum, thus paving the way towards the development of an autonomous implantable device for HS prevention.

Water Deprivation Induces Neurovascular and Cognitive Dysfunction through Vasopressin-Induced Oxidative Stress

Adequate hydration is essential for normal brain function and dehydration induces cognitive deterioration. In addition, dehydration has emerged as a stroke risk factor. However, it is unknown whether alterations in cerebrovascular regulation are responsible for these effects. To address this issue, C57Bl/6 mice were water deprived for 24 or 48 hours and somatosensory cortex blood flow was assessed by laser-Doppler flowmetry in a cranial window. Dehydration increased plasma osmolality and vasopressin levels, and suppressed the increase in blood flow induced by neural activity, by the endothelium-dependent vasodilator acetylcholine and the smooth muscle relaxant adenosine. The cerebrovascular dysfunction was associated with oxidative stress and cognitive deficits, assessed using the Y maze. The vasopressin 1a receptor antagonist SR49059 improved the dehydration-induced oxidative stress and vasomotor dysfunction. Dehydration upregulated endothelin-1 in cerebral blood vessels, an effect blocked by SR49059. Furthermore, the endothelin A receptor antagonist BQ123 ameliorated cerebrovascular function. These findings show for the first time that dehydration alters critical mechanisms regulating the cerebral circulation through vasopressin and oxidative stress. The ensuing cerebrovascular dysregulation may alter cognitive function and increase the brain's susceptibility to cerebral ischemia.

Mechanisms Involved in Dual Vasopressin/Apelin Neuron Dysfunction during Aging

Normal aging is associated with vasopressin neuron adaptation, but little is known about its effects on the release of apelin, an aquaretic peptide colocalized with vasopressin. We found that plasma vasopressin concentrations were higher and plasma apelin concentrations lower in aged rats than in younger adults. The response of AVP/apelin neurons to osmotic challenge was impaired in aged rats. The overactivity of vasopressin neurons was sustained partly by the increased expression of Transient receptor potential vanilloid2 (Trpv2), because central Trpv blocker injection reversed the age-induced increase in plasma vasopressin concentration without modifying plasma apelin concentration. The morphofunctional plasticity of the supraoptic nucleus neuron-astrocyte network normally observed during chronic dehydration in adults appeared to be impaired in aged rats as well. IL-6 overproduction by astrocytes and low-grade microglial neuroinflammation may contribute to the modification of neuronal functioning during aging. Indeed, central treatment with antibodies against IL-6 decreased plasma vasopressin levels and increased plasma apelin concentration toward the values observed in younger adults. Conversely, minocycline treatment (inhibiting microglial metabolism) did not affect plasma vasopressin concentration, but increased plasma apelin concentration toward control values for younger adults. This study is the first to demonstrate dual vasopressin/apelin adaptation mediated by inflammatory molecules and neuronal Trpv2, during aging.

Intranasal Angiotensin II in Humans Reduces Blood Pressure When Angiotensin II Type 1 Receptors Are Blocked

Intranasal administration of angiotensin II (ANGII) affects blood pressure in a mode different from intravenously administered ANGII via a direct access to the brain bypassing the blood-brain barrier. This clinical study investigated blood pressure regulation after intranasal ANGII administration in healthy humans, whereas systemic, blood-mediated effects of ANGII were specifically blocked. In a balanced crossover design, men (n=8) and women (n=8) were intranasally administered ANGII (400 μg) or placebo after ANGII type 1 receptors had been blocked by pretreatment with valsartan (80 mg; 12 and 6 hours before intranasal administration). Plasma levels of ANGII, aldosterone, renin, vasopressin, and norepinephrine were measured; blood pressure and heart rate were recorded continuously. Intranasal ANGII acutely decreased blood pressure without altering the heart rate. Plasma levels of vasopressin and norepinephrine remained unaffected. Plasma ANGII levels were increased throughout the recording period. Aldosterone levels increased despite the peripheral ANGII type 1 receptor blockade, indicating an aldosterone escape phenomenon. In conclusion, intranasal ANGII reduces blood pressure in the presence of selective ANGII type 1 receptor blockade. Intranasal ANGII administration represents a useful approach for unraveling the role of this peptide in blood pressure regulation in humans.

Workers exposed to urban stressors and the effects on antidiuretic hormone secretion.

The aim of this study was to evaluate whether urban pollutants can affect plasma levels of antidiuretic hormone (ADH) in outdoor workers. We selected 208 subjects, 104 exposed to urban stressors and 104 non exposed to urban stressors. We divided these workers in 3 groups: Group 1 (non-smokers and non-drinkers), Group 2 (smokers and not drinkers) and Group 3 (drinkers and not smokers). The means and standard deviations of ADH were calculated, and a Student's t-test was used to compare means. The data were considered significant at p ≤ 0.05. The outdoor workers in Group 1 had significantly reduced plasma levels of ADH. In contrast, the outdoor workers in Groups 2 and 3 had increased plasma levels of ADH. These results were consistent in both men and women. The results suggest that urban pollutants may influence the secretion of ADH.

The comparison of the effects of acute and repeated morphine administration on fast synaptic transmission in magnocellular neurons of supraoptic nucleus, plasma vasopressin levels, and urine volume of male rats.

The activity of the magnocellular neurons (MCNs) of supraoptic nucleus (SON) is regulated by a variety of excitatory and inhibitory inputs. Opioids are one of the important compounds that affect these inputs at SON synapses. In this study, whole-cell patch clamp recording of SON neurons was used to investigate the effect of acute and repeated morphine administration on spontaneous inhibitory and excitatory post synaptic currents (sIPSCs and sEPSCs) in MCNs. While acute bath application of morphine to brain slice of intact rat produced an increase in sEPSCs frequency and a decrease in sIPSCs frequency, repeated in-vivo administration of morphine produced opposite effect. Moreover, repetitive i.c.v. administration of morphine for three consecutive days caused significant increase in urine volume, but had no significant alteration in water consumption compared to control group. The increase in urine volume was consistent with a significant decrease in plasma arginine vasopressin (AVP) levels after repetitive i.p. morphine administration. The results suggest that acute administration of morphine stimulates whereas repeated administration of morphine inhibits the MCNs. Morphine-induced MCN inhibition could result in diminished plasma AVP levels and eventually an increase in urine volume of rats.

Roles of the subfornical organ and area postrema in arterial pressure increases induced by 48-h water deprivation in normal rats.

In rats, water deprivation (WD) increases arterial blood pressure (BP) in part due to actions of elevated osmolality in the brain to increase vasopressin levels and sympathetic activity. However, the osmoreceptors that mediate this response have not been identified. To test the hypothesis that osmoregulatory circumventricular organs are involved, BP and heart rate (HR) were continuously recorded telemetrically during 48 h of WD in normal rats with lesions (x) or sham lesions (sham) of the subfornical organ (SFO) or area postrema (AP). Although WD increased BP in SFOx and SFOsham rats, no significant difference in the hypertensive response was observed between groups. HR decreased transiently but similarly in SFOx and SFOsham rats during the first 24 h of WD. When water was reintroduced, BP and HR decreased rapidly and similarly in both groups. BP (during lights off) and HR were both lower in APx rats before WD compared to APsham. WD increased BP less in APx rats, and the transient bradycardia was eliminated. Upon reintroduction of drinking water, smaller falls in both BP and HR were observed in APx rats compared to APsham rats. WD increased plasma osmolality and vasopressin levels similarly in APx and APsham rats, and acute blockade of systemic V1 vasopressin receptors elicited similar depressor responses, suggesting that the attenuated BP response is not due to smaller increases in vasopressin or osmolality. In conclusion, the AP, but not the SFO, is required for the maximal hypertensive effect induced by WD in rats.

Relation between Stress-Related Hormone and Sudden Sensorineural Hearing Loss

Received September 27, 2013 Revised February 10, 2014 Accepted February 12, 2014 Address for correspondence Byung don Lee, MD, PhD Department of OtolaryngologyHead and Neck Surgery, Soonchunhyang University College of Medicine, 59 Daesagwan-ro, Yongsan-gu, Seoul 140-743, Korea Tel +82-2-709-9363 Fax +82-2-709-9134 E-mail bdlee12@schmc.ac.kr Background and ObjectivesZZThe plasma stress-related hormonal [cortisol, growth hormone, prolactin, antidiuretic hormone (ADH), adrenocorticotropic hormone (ACTH)] levels have been reported to be elevated in sudden sensorineural hearing loss (SSNHL) patients. However, little is known regarding the mechanisms related with the elevation of stress-related hormonal levels in SSNHL. Therefore, we measured the level of plasma stress-related hormones in SSNHL patients and in normal persons to demonstrate the association between the stress-related hormones and SSNHL. Subjects and MethodZZStress-related hormonal levels were measured from 68 patients who were diagnosed with SSNHL. These values were compared with the stress-related hormonal levels of 24 healthy control subjects. ResultsZZThe plasma ADH levels was significantly higher in SSNHL group compared with that in their normal control group, as shown by their respective values, 4.46 [95% confidence interval (CI): 3.80-5.24 pg/mL] and 3.05 (95% CI: 2.34-3.98 pg/mL). The values for plasma cortisol, growth hormone, and ACTH levels whose values were 2.07 (95% CI: 1.65-2.61 μg/L), 0.20 (95% CI: 0.14-0.29 μg/L), and 12.79 (95% CI: 11.16-14.66 pg/mL), respectively, were significantly lower in the SSNHL group than those in the normal control group whose values were 7.86 (95% CI: 5.33-5.24 μg/L), 0.61 (95% CI: 0.36-1.04 μg/L), 18.48 (95% CI: 14.9922.78 pg/mL), respectively. But there was no significant difference in prolactin between the two groups. ConclusionZZThis study demonstrates a possible role of stress-related hormones in the pathogenesis of SSNHL. However, only ADH level was higher than the control group. Furthermore, ACTH, growth hormone and cortisol levels were lower than the control groups. This means ADH, growth hormone, cortisol, ACTH levels are related with SSNHL. However, the impact of this hormone on the inner ear and endolymph homeostasis is still unknown. Further investigation is necessary to identify the action mechanism of these hormones in the inner ear. Korean J Otorhinolaryngol-Head Neck Surg 2014;57(6):373-8