pituitrin and Cardiovascular-Diseases

Vasopressin concentration is typically higher at night, during stress, and in males, but readily lowered by water intake. Vasopressin is also a causal candidate for cardiometabolic disease, which shows seasonal variation.. To study whether vasopressin concentration varies by season in a temperate climate.. The vasopressin surrogate marker copeptin was analyzed in fasting plasma samples from five population-based cohorts in Malmö, Sweden (n = 25,907, 50.4% women, age 18-86 years). We investigated seasonal variation of copeptin concentration and adjusted for confounders in sinusoidal models.. The predicted median copeptin level was 5.81 pmol/L (7.18 pmol/L for men and 4.44 pmol/L for women). Copeptin exhibited a distinct seasonal pattern with a peak in winter (mid-February to mid-March) and nadir in late summer (mid-August to mid-September). The adjusted absolute seasonal variation in median copeptin was 0.62 pmol/L (95% confidence interval [CI] 0.50; 0.74, 0.98 pmol/L [95% CI 0.73; 1.23] for men and 0.46 pmol/L [95% CI 0.33; 0.59] for women). The adjusted relative seasonal variation in mean log copeptin z-score was 0.20 (95% CI 0.17; 0.24, 0.18 [95% CI 0.14; 0.23] in men and 0.24 [95% CI 0.19; 0.29] in women). The observed seasonal variation of copeptin corresponded to a risk increase of 4% for incident diabetes mellitus and 2% for incident coronary artery disease.. The seasonal variation of the vasopressin marker copeptin corresponds to increased disease risk and mirrors the known variation in cardiometabolic status across the year. Moderately increased water intake might mitigate the winter peak of cardiometabolic disease.

Topics: Adolescent; Adult; Aged; Aged, 80 and over; Biomarkers; Cardiovascular Diseases; Female; Glycopeptides; Humans; Male; Middle Aged; Seasons; Vasopressins; Young Adult

The automatism of cardiac pacemaker cells, which is tuned, is regulated by the autonomic nervous system (ANS) and multiple endocrine and paracrine factors, including cardiovascular peptides. The cardiovascular peptides (CPs) form a group of essential paracrine factors affecting the function of the heart and vessels. They may also be produced in other organs and penetrate to the heart via systemic circulation. The present review draws attention to the role of vasopressin (AVP) and some other cardiovascular peptides (angiotensins, oxytocin, cytokines) in the regulation of the cardiovascular system in health and cardiovascular diseases, especially in post-infarct heart failure, hypertension and cerebrovascular strokes. Vasopressin is synthesized mostly by the neuroendocrine cells of the hypothalamus. There is also evidence that it may be produced in the heart and lungs. The secretion of AVP and other CPs is markedly influenced by changes in blood volume and pressure, as well as by other disturbances, frequently occurring in cardiovascular diseases (hypoxia, pain, stress, inflammation). Myocardial infarction, hypertension and cardiovascular shock are associated with an increased secretion of AVP and altered responsiveness of the cardiovascular system to its action. The majority of experimental studies show that the administration of vasopressin during ventricular fibrillation and cardiac arrest improves resuscitation, however, the clinical studies do not present consisting results. Vasopressin cooperates with the autonomic nervous system (ANS), angiotensins, oxytocin and cytokines in the regulation of the cardiovascular system and its interaction with these regulators is altered during heart failure and hypertension. It is likely that the differences in interactions of AVP with ANS and other CPs have a significant impact on the responsiveness of the cardiovascular system to vasopressin in specific cardiovascular disorders.

Topics: Angiotensins; Arginine Vasopressin; Cardiovascular Diseases; Cardiovascular System; Cytokines; Heart Failure; Humans; Hypertension; Lung; Oxytocin; Vasopressins

Arginine vasopressin (AVP), which is also called antidiuretic hormone (ADH), is a neurohormone synthetized from a pre-pro-hormone precursor in the supraoptic and paraventricular nuclei of the hypothalamus in response to increased plasma osmolality and decreased blood volume. AVP exerts several effects by binding to three different receptors: V1aR, V1bR, and V2R. In recent years, it has been suggested that increased plasma concentration of AVP may play a causal role in the development of type 2 diabetes, the metabolic syndrome, renal dysfunction and cardiovascular disease by influencing glucose homeostasis and lipid metabolism through several possible mechanisms involving V1aR and V1bR. V1aR located in the liver is involved in hepatic glycogenolysis and gluconeogenesis. V1bR, found in the pituitary gland and pancreas, mediates secretion of adrenocorticotrophic hormone (ACTH), insulin, and glucagon. However, AVP's clinical use as a biomarker is limited due to its short half-life in plasma (16-20 minutes), small size, and poor stability, which make direct measurement difficult. Copeptin, the biologically inactive, stable, C-terminal part of pro-vasopressin, is co-secreted with AVP in equimolar amounts and thus is considered an adequate and clinically useful surrogate marker of AVP. The aim of this review is to assess the current state of knowledge about the potential role of copeptin as a novel biomarker of cardiometabolic syndrome on the basis of recent scientific literature published up to December 2020 and searches of the PubMed, Google Scholar, and Web of Science databases.

Topics: Arginine Vasopressin; Biomarkers; Cardiovascular Diseases; Diabetes Mellitus, Type 2; Glycopeptides; Humans; Metabolic Syndrome; Neurophysins; Predictive Value of Tests; Protein Precursors; Vasopressins

Copeptin, arginine vasopressin (AVP)-associated 39 aminoacid glycopeptide, is a C-terminal part of pro-AVP. AVP acts through V1a, V1b, and V2 receptors. The effect on V1a receptors is connected with arterial vasoconstriction, on V2 with antidiuretic action, and on V1b with the secretion of ACTH, insulin, glucagon. Copeptin is found in the circulation in equimolar amounts with AVP. It is a very stable peptide and easy to estimate. Copeptin is a good diagnostic marker in many disorders in which vasopressinergic dysfunction plays a role in pathogenesis such as a polyuria-polydipsia syndrome, neurological disease (ischemic stroke, nontraumatic, intracerebral hemorrhage, aneurysmal subarachnoid hemorrhage and neurodegenerative disease (multiple sclerosis). Copeptin is a diagnostic and prognostic marker in cardiovascular diseases like heart failure (HF) and acute myocardial infarct (AMI). Copeptin is a sensitive diagnostic marker in the early stage of AMI especially in patients with non-ST segment elevation and post AMI complications. Copeptin is also an important diagnostic and prognostic marker in metabolic diseases (diabetes mellitus, metabolic syndrome, insulin resistance), connected with some neurological and cardiovascular diseases. In the future, these findings may have also therapeutic applications in conditions where the AVP receptor antagonist therapy is appropriate.

Topics: Biomarkers; Cardiovascular Diseases; Glycopeptides; Humans; Nervous System Diseases; Neurophysins; Predictive Value of Tests; Prognosis; Protein Precursors; Vasopressins

Chronic kidney disease (CKD) imposes a significant global health burden. In the United States, one in three adults are at risk for CKD currently affecting over 28 million Americans. While several studies have demonstrated the benefit of treating traditional risk factors in CKD, including hypertension with pharmacologic agents such as blockade of the renin-angiotensin system (RAAS), there is scarce data on the advantages of sodium and fluid management in this population. Both experimental and observational studies have shown improvement in hypertension and cardiovascular outcomes with sodium restriction to ≤2.3 grams per day, however, to date there are very few randomized controlled trials demonstrating a benefit in sodium reduction for the prevention or progression of CKD. Similarly, studies on increasing fluid consumption have shown to be advantageous in polycystic kidney disease as well as chronic nephrolithiasis, yet no randomized controlled trials exist on the fluid management in patients with kidney disease. This review aims to explore the evidence of sodium restriction and fluid management in the CKD population as well as underlying mechanisms and clinical barriers of sodium and water management as conservative therapy.

Topics: Angiotensin-Converting Enzyme Inhibitors; Cardiovascular Diseases; Conservative Treatment; Disease Progression; Fluid Therapy; Humans; Hypertension; Hypertrophy, Left Ventricular; Hyponatremia; Polycystic Kidney Diseases; Renal Insufficiency, Chronic; Renin-Angiotensin System; Risk Factors; Sodium Chloride; United States; Vasopressins

Research studies indicate a role of the apelinergic and vasopressinergic systems both in the regulation of the cardiovascular system and the pathogenesis of CVD, including in such settings as obesity and stress. Based on these data, it may be suggested that interactions between these systems underlie numerous physiological and pathophysiological processes, some of them related to the cardiovascular system. Better understanding of the role of these systems and their interactions, both physiological and related to the pathogenesis of CVD, will allow further advances in prevention and drug therapy.

Topics: Cardiovascular Diseases; Cardiovascular System; Humans; Intercellular Signaling Peptides and Proteins; Vasoconstrictor Agents; Vasopressins

Orthostatic hypotension (OH) is defined as a decrease in systolic blood pressure of 20 mmHg, or a decrease in diastolic blood pressure of 10 mmHg within three minutes of standing. It results from an inadequate response to postural changes in blood pressure. Common symptoms include dizziness, light-headedness, blurred vision, weakness, fatigue, nausea, palpitations, sweating, head and neck ache, slow cognitive performance and transient loss of conscientiousness. OH is a common problem among elderly patients and its aetiology is diverse, including autonomic nervous system dysfunction, cardiac problems, medication side effects, ageing changes or transitory deregulation of blood volume. The instrumental diagnosis can be easily accomplished by the tilt-table test, with continuous monitoring of blood pressure and cardiac parameters. It is a non-invasive technique and needs minimal collaboration from the patient. In our experience, when reviewing 327 patients, aged over 40 years and examined because of clinical suspicion of OH, the prevalence thereof was 51% whereas if focused in subjects older than 70, OH was proven in 90% of the cases. The older the patients, the more frequently they presented general deterioration, neurological or cardiac problems as well as pharmacological side effects. Ruling out neurological or cardiac malfunction can drastically improve the prognosis with possible reversibility of symptoms. Some nonpharmacological and pharmacological approaches to improve management of OH and life quality are described for guidance.

Topics: Adult; Age of Onset; Aged; Aged, 80 and over; Autonomic Nervous System Diseases; Cardiovascular Diseases; Central Nervous System Stimulants; Dehydration; Diagnostic Techniques, Neurological; Fludrocortisone; Fluid Therapy; Humans; Hypotension, Orthostatic; Metabolic Diseases; Middle Aged; Stockings, Compression; Sympathomimetics; Vasopressins

The renin angiotensin system (RAS) is a peptide hormone system that plays an important role in the pathophysiology of various diseases, including congestive heart failure, hypertension, myocardial infarction, and diabetic nephropathy. This has led researchers to focus extensively on this system, leading to the discovery of various peptides, peptidases, receptors and signal transduction mechanisms intrinsic to the RAS. Angiotensinogen (AGT), angiotensin (Ang) II, Ang III, Ang IV, and Ang-(1-7) are the main biologically active peptides of RAS. However, most of the available studies have focused on Ang II as the likely key peptide from the RAS that directly and indirectly regulates physiological functions leading to pathological conditions. However, data from recent studies suggest that Ang III may produce physiologically relevant effects that are similar to those produced by Ang II. Hence, this review focuses on Ang III and the myriad of physiological effects that it produces in the body.

Topics: Angiotensin III; Animals; Atrial Natriuretic Factor; Blood Pressure; Blood Volume; Cardiovascular Diseases; Diabetic Neuropathies; Humans; Rats; Renin-Angiotensin System; Signal Transduction; Sodium; Thirst; Vasopressins

Orthostatic hypertension-a condition characterized by a hyperactive pressor response to orthostatic stress-is an emerging risk factor for cardiovascular disease and is associated with hypertensive target-organ damage (resulting in silent cerebrovascular disease, left ventricular hypertrophy, carotid atherosclerosis and/or chronic kidney disease) and cardiovascular events (such as coronary artery disease and lacunar stroke). The condition is also considered to be a form of prehypertension as it precedes hypertension in young, normotensive adults. Orthostatic blood pressure changes can be assessed using orthostatic stress tests, including clinic active standing tests, home blood pressure monitoring and the head-up tilting test. Devices for home and for ambulatory blood pressure monitoring that are equipped with position sensors and do not induce a white-coat effect have increased the sensitivity and specificity of diagnosis of out-of-clinic orthostatic hypertension. Potential major mechanisms of orthostatic hypertension are sympathetic hyperactivity (as a result of hypersensitivity of the cardiopulmonary and arterial baroreceptor reflex) and α-adrenergic hyperactivation. Orthostatic hypertension is also associated with morning blood pressure surge and extreme nocturnal blood pressure dipping, both of which increase the pulsatile haemodynamic stress of central arterial pressure and blood flow in patients with systemic haemodynamic atherothrombotic syndrome.

Topics: Age Factors; Arteriosclerosis; Blood Pressure Monitoring, Ambulatory; Blood Volume; Brain Infarction; Cardiovascular Diseases; Diabetes Mellitus; Hemodynamics; Humans; Hypertriglyceridemia; Hypotension, Orthostatic; Posture; Prehypertension; Receptors, Adrenergic, alpha; Renal Insufficiency, Chronic; Risk Factors; Sympathetic Nervous System; Thrombosis; Tilt-Table Test; Vasopressins; Ventricular Remodeling

Biomarkers have been intensively studied in community-acquired pneumonia (CAP) in recent years. In the context of the CAPNETZ study we had the unique opportunity to evaluate old and new biomarkers in a multicentre study with a high number of patients.. In several substudies we found the following results: procalcitonin, CRP and leukocytes show highest values in patients with typical bacterial etiology of CAP, but do not allow individual prediction of etiology. Patients without antibiotic pre-treatment show higher values of biomarkers compared to patients with antibiotic pre-treatment. New cardiovascular biomarkers are good predictors for short- and long-term mortality in CAP, superior to the inflammatory markers procalcitonin, CRP and leukocytes and at least comparable to the clinical CRB-65 score. Pro-Adrenomedullin is among the new biomarkers the one with the best prognostic value.. Biomarkers correlate with the severity of CAP but do not allow individual prediction of etiology. New cardiovascular biomarkers are suitable for the evaluation of short- and long-term prognosis in CAP. The combination of several biomarkers reflecting different pathophysiological pathways has the potential to improve management of CAP in the future.

Topics: Adolescent; Adrenomedullin; Adult; Age Distribution; Aged; Aged, 80 and over; Atrial Natriuretic Factor; Biomarkers; Blood Pressure; C-Reactive Protein; Calcitonin; Calcitonin Gene-Related Peptide; Cardiovascular Diseases; Community-Acquired Infections; Comorbidity; Endothelin-1; Female; Germany; Humans; Inflammation; Leukocyte Count; Male; Middle Aged; Pneumonia; Predictive Value of Tests; Protein Precursors; Respiratory Rate; Survival Analysis; Vasopressins; Young Adult

With increases in use of regional anesthesia, local anesthetic systemic toxicity (LAST) has been a topic of interest and debate. Despite many years of research, the exact cause and best treatment of LAST (particularly local anesthetic cardiotoxicity) remain unclear. This review will summarize what is known and what remains uncertain about LAST and its treatment, including information published in the past 12-18 months.. Several authorities, including the American Society of Regional Anesthesia and Pain Medicine, have published guidelines on prevention and treatment of LAST. Experimental data continue to add to better understanding of LAST and its treatment. The data are not entirely consistent, but themes include continued evidence to support the ideas that LAST cardiotoxicity occurs primarily at sodium channels, lipid emulsion is a reasonably well tolerated and effective treatment, and there may be qualitative differences in cardiotoxicity caused by low and high-potency local anesthetics.. Regarding mechanism(s) of LAST, the evidence remains mixed, but it is likely that local anesthetic cardiotoxicity primarily arises from a blockade of sodium channels. As for treatment, in addition to ventilation, oxygenation, and chest compressions, lipid emulsion therapy should be a primary element in the treatment of cardiovascular LAST. The use of epinephrine and vasopressin should be tailored to specifics of an episode of LAST, and doses should be kept as low as possible while still achieving the desired effects.

Topics: Anesthesia, Local; Anesthetics, Local; Animals; Bupivacaine; Cardiovascular Diseases; Disease Models, Animal; Epinephrine; Fat Emulsions, Intravenous; Humans; Lidocaine; Neurotoxicity Syndromes; Vasoconstrictor Agents; Vasopressins

Topics: Animals; Cardiovascular Diseases; Humans; Hypothalamic Hormones; Osmolar Concentration; Signal Transduction; Vasopressins

Hospitalization for heart failure is a major health problem with high in-hospital and postdischarge mortality and morbidity. Non-potassium-sparing diuretics (NPSDs) still remain the cornerstone of therapy for fluid management in heart failure despite the lack of large randomized trials evaluating their safety and optimal dosing regimens in both the acute and chronic setting. Recent retrospective data suggest increased mortality and re-hospitalization rates in a wide spectrum of heart failure patients receiving NPSDs, particularly at high doses. Electrolyte abnormalities, hypotension, activation of neurohormones, and worsening renal function may all be responsible for the observed poor outcomes. Although NPSD will continue to be important agents to promptly resolve signs and symptoms of heart failure, alternative therapies such as vasopressine antagonists and adenosine blocking agents or techniques like veno-venous ultrafiltration have been developed in an effort to reduce NPSD exposure and minimize their side effects. Until other new agents become available, it is probably prudent to combine NPSD with aldosterone blocking agents that are known to improve outcomes.

Topics: Adenosine; Cardiovascular Diseases; Heart Failure; Hemofiltration; Hormone Antagonists; Humans; Kidney Diseases; Risk Assessment; Risk Factors; Sodium Potassium Chloride Symporter Inhibitors; Time Factors; Treatment Outcome; Vasopressins; Water-Electrolyte Balance

Arginine vasopressin (AVP or antidiuretic hormone) is one of the key hormones in the human body responsible for a variety of cardiovascular and renal functions. It has so far escaped introduction into the routine clinical laboratory due to technical difficulties and preanalytical errors. Copeptin, the C-terminal part of the AVP precursor peptide, was found to be a stable and sensitive surrogate marker for AVP release. Copeptin behaves in a similar manner to mature AVP in the circulation, with respect to osmotic stimuli and hypotension. During the past years, copeptin measurement has been shown to be of interest in a variety of clinical indications, including cardiovascular diseases such as heart failure, myocardial infarction, and stroke. This review summarizes the recent progress on the diagnostic use of copeptin in cardiovascular and renal diseases and discusses the potential use of copeptin measurement in the context of therapeutic interventions with vasopressin receptor antagonists.

Topics: Arginine Vasopressin; Biomarkers; Blood Volume; Cardiovascular Diseases; Cardiovascular System; Glycopeptides; Heart Failure; Humans; Kidney; Kidney Diseases; Myocardial Infarction; Prognosis; ROC Curve; Shock, Cardiogenic; Stroke; Vasopressins

The vasopressin system is complex and interacts with the central nervous, cardiovascular, renal, and hematological systems. Vasopressin plays an important role in the control of blood osmolarity and vascular tone, but is also involved in many other physiological events, which are mediated mainly via three types of vasopressin receptor: V1R, V2R, and V3R. V1R primarily mediate the vascular, and V2R the aquaretic, effects of vasopressin. Vasopressin may also interact with other receptors, like adrenergic and angiotensin-II receptors, or with distinct biological pathways, including those of nitric oxide and the K(ATP) channel. There are numerous clinical situations where vasopressin receptor modulators (agonists or antagonists) could be used. Currently, vasopressin and terlipressin are most commonly used to stimulate V1R in vasodilatory shock and cardiac arrest, while desmopressin, a synthetic analogue of vasopressin, acts on V2R; but new molecules are becoming available in the treatment of inappropriate antidiuretic hormone (ADH) secretion.

Topics: Animals; Antidiuretic Hormone Receptor Antagonists; Brain Diseases; Cardiovascular Diseases; Clinical Trials as Topic; Drugs, Investigational; Hemorrhage; Humans; Inappropriate ADH Syndrome; Receptors, Vasopressin; Skin Diseases; Vasopressins

Effects of vasopressin via V1a- and V2-receptors are closely implicated in a variety of water-retaining diseases and cardiovascular diseases, including heart failure, hyponatraemia, hypertension, renal diseases, syndrome of inappropriate antidiuretic hormone secretion, cirrhosis and ocular hypertension. As vasopressin receptors are found in many different tissues, vasopressin antagonists may benefit the treatment of disorders such as cerebral ischaemia and stroke, Raynaud's disease, dysmenorrhoea and tocolytic treatment. V1b selective vasopressin antagonists are discussed in terms of their usefulness in the treatment of emotional and psychiatric disorders. The vaptans are vasopressin receptor antagonists with V1a (relcovaptan) or V2 (tolvaptan, lixivaptan) selectivity or non-selective activity (conivaptan) which may be advantageous in some disorders. The V1a/V2 non-selective vasopressin antagonist conivaptan is the first vaptan which is approved by the FDA for the treatment of euvolaemic hyponatraemia.

Topics: Animals; Antidiuretic Hormone Receptor Antagonists; Azepines; Benzamides; Benzazepines; Binding Sites; Cardiovascular Diseases; Clinical Trials as Topic; Hormone Antagonists; Humans; Indoles; Pyrroles; Pyrrolidines; Tolvaptan; Vasopressins; Water-Electrolyte Imbalance

Growing number of studies reveal that the brain neural network plays significant role in the short-term and long-term regulation of the cardiovascular functions. The neurons involved in the complex neurogenic control of the cardiovascular system use classical neurotransmitters and nonconventional mediators such as peptides (angiotensin II, vasopressin, natriuretic peptides, endothelins, opioids, cytokines), steroids, ouabain-like factors and gaseous compounds. Among them the neuropeptides form a group of substances arising significant interest. Thanks to wide distribution of peptidergic neurons in the central nervous system, location of peptide receptors on neurons and glial cells, versatile but frequently overlapping mechanisms of activation of the intracellular processes the neuropeptides play significant role in short-term and long-term regulation of excitability and remodeling of the neurons. In several instances they modulate effects of the classical transmitting systems involved in regulation blood pressure, heart rate, water-electrolyte balance, metabolism, stress, pain, mood and memory. Prolonged activation or inhibition of specific neuropeptide pathways frequently results in long-lasting disorders of several regulatory systems. In this review this is exemplified by overactivity of angiotensin II, vasopressin and cytokines in the brain during hypertension, heart failure and stress. Multifarious actions of angiotensin II and vasopressin, and their mutual interaction with cytokines make of these neuropeptides excellent candidates for the compounds responsible for long-term resetting of the central cardiovascular control, and forming a link between the cardiovascular diseases, stress and mood disorders.

Topics: Angiotensin II; Brain; Cardiovascular Diseases; Cardiovascular Physiological Phenomena; Cytokines; Heart Failure; Humans; Hypertension; Nerve Net; Neuropeptides; Neurosecretory Systems; Stress, Psychological; Vasopressins

Cushing's syndrome is a consequence of primary or, more commonly, secondary oversecretion of cortisol. Cardiovascular disease is the major cause of morbidity and mortality in Cushing's syndrome, and excess risk remains even in effectively treated patients. The cardiovascular consequences of cortisol excess are protean and include, inter alia, elevation of blood pressure, truncal obesity, hyperinsulinemia, hyperglycemia, insulin resistance, and dyslipidemia. This review analyses the relationship of cortisol excess, both locally and at tissue level, to these cardiovascular risk factors, and to putative mechanisms for hypertension. Previous studies have examined correlations between cortisol, blood pressure, and other parameters in the general population and in Cushing's syndrome. This review also details changes induced by short-term cortisol administration in normotensive healthy men.

Topics: Blood Pressure; Cardiac Output; Cardiovascular Diseases; Cushing Syndrome; Female; Humans; Hydrocortisone; Hyperglycemia; Hyperlipidemias; Hypertension; Insulin Resistance; Male; Obesity; Plasma Volume; Renin-Angiotensin System; Risk Factors; Sympathetic Nervous System; Vascular Resistance; Vasodilation; Vasopressins

Vasopressin is a vital homeostatic protein which regulates fluid balance via its antidiuretic effects and vascular tone via its vasoconstrictive effects. Endogenous vasopressin deficiency has been implicated in several disease states resulting in vasodilatory shock. In particular, vasopressin levels are low in patients following cardiac surgery and in those with ventricular dysrhythmias. Several recent studies have demonstrated the effectiveness of exogenous vasopressin in providing haemodynamic support in patients with postcardiopulmonary bypass vasodilatory shock and refractory ventricular fibrillation. This manuscript reviews the pathophysiological and clinical basis for vasopressin replacement in patients with cardiovascular collapse.

Topics: Cardiopulmonary Resuscitation; Cardiovascular Diseases; Deamino Arginine Vasopressin; Hemostatics; Humans; Postoperative Period; Vasopressins

The circulation is controlled by overlapping haemodynamic, structural and neurohumoral mechanisms. Many hormonal vasoactive substances, mostly derived from endothelial cells, are also growth regulators. Although neurohormonal systems are involved in normal physiological compensatory responses they often become maladaptive in conditions such as congestive heart failure. The success of blocking the renin angiotensin system by angiotensin converting enzyme (ACE) inhibitors has led to efforts to block other hormonal systems. Neutral endopeptidase (NEP), the major enzymatic pathway for degradation of natriuretic peptides, has a similar catalytic site to ACE. This has led to compounds that simultaneously inhibit both enzymes. Such dual ACE/NEP inhibitors show promise in experimental hypertension and heart failure. Similar dual NEP/ECE (endothelin converting enzyme) inhibitors are becoming available. The hormone vasopressin has dual actions on the vasculature and the kidney via specific membrane receptors. Specific orally active vasopressin receptor antagonists have been developed and their therapeutic potential in hypertension, heart failure and oedematous states are being explored.

Topics: Angiotensin-Converting Enzyme Inhibitors; Animals; Cardiovascular Diseases; Hormone Antagonists; Humans; Metalloendopeptidases; Peptides; Vasopressins

Infants and children with congenital or acquired heart disease and children with systemic disease often require pharmacological support of their failing circulation. Catecholamines may serve as inotropic (enhance myocardial contractility) or vasopressor (elevate systemic vascular resistance) agents. Noncatecholamine inotropic agents, such as the cardiac glycosides or the bipyridines, may be used in place of, or in addition to, catecholamines. Developmental changes in neonates, infants and children will affect the response to inotropic or pressor therapy. Maturation of the gastrointestinal tract, liver and kidneys alters absorption, metabolism and elimination of drugs, although there are few clear examples of this among the vasoactive drugs considered in this review. Changes in body composition affect the volume of distribution (Vd) and clearance (CL) of drugs. Developmentally based pharmacodynamic differences also affect the responses to both therapeutic and toxic effects of inotropes. These pharmacodynamic differences are based in part upon developmental changes in myocardial structure, cardiac innervation and adrenergic receptor function. For example, the immature myocardium has fewer contractile elements and therefore a decreased ability to increase contractility; it also responds poorly to standard techniques of manipulating preload. Available data suggest that dopamine and dobutamine pharmacokinetics are similar to those in adults. Wide interindividual variability has been noted. A consistent relationship between CL and age has not been demonstrated, although one investigator demonstrated an almost 2-fold increase in the CL of dopamine in children under the age of 2 years. The CL of dopamine appears to be reduced in children with renal and hepatic failure. Fewer data are available regarding the pharmacokinetics of epinephrine (adrenaline), norepinephrine (noradrenaline) and isoprenaline (isoproterenol). Digoxin pharmacokinetics have been extensively evaluated in infants and children. The Vd for digoxin is increased in infants and children. Children beyond the neonatal period display increased CL of digoxin, approaching adult values during puberty. Although it was previously thought that children both needed and tolerated higher serum concentrations of digoxin than adults, more recent studies indicate that adequate clinical response can be achieved with serum concentrations similar to those aimed for in adults, with decreased toxicity. Evaluation of s

Topics: Animals; Cardiotonic Agents; Cardiovascular Diseases; Catecholamines; Child, Preschool; Humans; Infant; Infant, Newborn; Vasopressins

Topics: Adrenal Cortex Hormones; Arrhythmias, Cardiac; Cardiovascular Diseases; Catecholamines; Cerebrovascular Disorders; Humans; Hyperglycemia; Hypertension; Hyponatremia; Models, Biological; Pulmonary Edema; Vasopressins

Topics: Adrenocorticotropic Hormone; Adult; Alkalosis, Respiratory; Anaphylaxis; Animals; Cardiovascular Diseases; Collagen Diseases; Gastrointestinal Diseases; Gonadotropins; Hematologic Diseases; Hormones, Ectopic; Humans; Hypoxia; In Vitro Techniques; Infant, Newborn; Lung; Lung Diseases; Lung Neoplasms; Microscopy, Electron; Neuromuscular Diseases; Neurotransmitter Agents; Paraneoplastic Endocrine Syndromes; Pulmonary Edema; Pulmonary Embolism; Pulmonary Emphysema; Rats; Respiratory Distress Syndrome, Newborn; Skin Diseases; Syndrome; Vasopressins

Topics: Aging; Angiotensin II; Animals; Atropine; Bartter Syndrome; Bone and Bones; Carbohydrate Metabolism; Cardiovascular Diseases; Drug Hypersensitivity; Gastric Mucosa; Gastrointestinal Diseases; Heart; Hematologic Diseases; Humans; Kidney Failure, Chronic; Parathyroid Diseases; Parathyroid Hormone; Pharmaceutical Preparations; Rabbits; Rats; Thyroid Diseases; Uremia; Vasopressins; Vitamin D

Topics: Anesthesia, Dental; Anesthesia, General; Anesthesia, Local; Antidepressive Agents; Antihypertensive Agents; Cardiovascular Diseases; Catecholamines; Desoxycorticosterone; Diazepam; Drug Synergism; Epinephrine; Humans; Hyperthyroidism; Norepinephrine; Oral Hemorrhage; Vasoconstrictor Agents; Vasopressins

Topics: Adrenal Cortex Hormones; Adult; Analgesics; Antifibrinolytic Agents; Blood Transfusion; Cardiovascular Diseases; Child; Contraceptives, Oral; Estrogens; Factor IX; Factor VIII; Gastrointestinal Diseases; Hemarthrosis; Hemophilia A; Hemophilia B; Hemorrhage; Home Nursing; Humans; Infections; Inhalation; Nervous System Diseases; Social Adjustment; Thyroxine; Triiodothyronine; Urologic Diseases; Vasopressins

Topics: Acetylcholine; Adjuvants, Anesthesia; Adrenal Cortex Hormones; Anesthesia; Blood Circulation; Cardiac Output; Cardiovascular Diseases; Cardiovascular Physiological Phenomena; Cardiovascular System; Epinephrine; Heart; Heart Diseases; Humans; Myocardium; Norepinephrine; Thyroid Hormones; Vasopressins

Using data from the multicenter, observational Diast-CHF (Diagnostic Trial on Prevalence and Clinical Course of Diastolic Dysfunction and Heart Failure) study, this post-hoc analysis aimed at assessing the association between serum concentrations of C-terminal pro-arginine vasopressin (CT-proAVP) and anxiety in patients with cardiovascular risk factors.. Animal studies have demonstrated that centrally released AVP is involved in the development of anxiety-like behaviors, however, it is unknown whether, also in humans, CT-proAVP used as a proxy for the co-secreted AVP is associated with self-reported anxiety.. In 1463 study participants with cardiovascular risk factors (mean age 66.7 ± 8.1 years, 51.3% males, mean left ventricular ejection fraction 59.8 ± 8.3%), serum concentrations of CT-proAVP were measured by means of an ELISA assay, and anxiety was assessed using the Hospital Anxiety and Depression Scale (HADS).. Data showed that there was a significant and inverse correlation between HADS anxiety and CT-proAVP (rho = -0.074; p = 0.005). Serum CT-proAVP and the HADS anxiety differed between the two sexes: men displayed lower anxiety (4.7 ± 3.5 versus 5.5 ± 3.7) and had higher CT-proAVP levels (5.8 pmol/L, interquartile range 3.5-9.9 pmol/L versus 3.0 pmol/L, interquartile range 2.0-4.7) than women (both, p < 0.001). Using univariate ANOVA adjusted for age, body-mass index, estimated glomerular filtration rate, left ventricular ejection fraction, 6-minute walking distance, SF-36 physical functioning, and the natriuretic peptides NT-proBNP and MR-proANP, the interaction term sex*CT-proAVP was significantly associated with anxiety (p = 0.006). Further analysis showed that CT-proAVP was inversely related to anxiety only in men (B = -0.991; 95%CI = -1.650 to -0.331; p = 0.003), but not in women (p = 0.335).. In male study participants with cardiovascular risk factors, serum concentrations of CT-proAVP showed an inverse association with anxiety, which was independent from the severity of physical impairment.

Topics: Aged; Anxiety; Anxiety Disorders; Arginine Vasopressin; Biomarkers; Cardiovascular Diseases; Cardiovascular System; Female; Humans; Male; Middle Aged; Neurophysins; Prognosis; Protein Precursors; Risk Factors; Sex Factors; Tomography, X-Ray Computed; Vasopressins

Type 2 diabetes, chronic kidney disease (CKD) and its cardiovascular complications are increasing as health problems worldwide. These diseases are interrelated with overlapping occurrence and once diabetes is established, the risk of cardiorenal disease is dramatically elevated. Thus, a search for unifying modifiable risk factors is key for effective prevention.. Elevated fasting plasma concentration of vasopressin, measured with the marker copeptin, predicts new onset type 2 diabetes as well as renal function decline. Furthermore, we recently showed that increased plasma copeptin concentration independently predicts the development of both CKD and other specified kidney diseases. In consequence, high copeptin is an independent risk factor for cardiovascular disease and premature mortality in both diabetes patients and in the general population. Vasopressin is released when plasma osmolality is high, and the easiest way to lower plasma vasopressin and copeptin concentration is to increase water intake. In a human water intervention experiment with 1 week of 3 L/day increased water intake, the one third of the participants with the greatest copeptin reduction (water responders) were those with a phenotype of low water intake (high habitual plasma copeptin and urine osmolality, and low urine volume). The water-responders had a copeptin reduction of 41% after 1 week of increased water intake compared to a control week; in contrast, a 3% reduction occurred in the other two thirds of the study participants. Among water responders, increased water intake also induced a reduction in fasting glucagon concentration. Key Messages: Elevated copeptin, a measure of vasopressin, is a risk marker of metabolic and cardiorenal diseases and may assist in the detection of individuals at higher risk for these diseases. Furthermore, individuals with high copeptin and other signs of low water intake may experience beneficial glucometabolic effects of increased water intake. Future randomized control trials investigating effects of hydration on glucometabolic and renal outcomes should focus on individuals with signs of low water intake including high plasma copeptin concentration.

Topics: Cardiovascular Diseases; Diabetes Mellitus, Type 2; Drinking; Glycopeptides; Humans; Life Style; Osmolar Concentration; Renal Insufficiency, Chronic; Risk Factors; Vasopressins

Topics: Antidiuretic Hormone Receptor Antagonists; Cardiovascular Diseases; Congresses as Topic; Glycopeptides; Humans; Kidney; Kidney Diseases; Liver; Metabolic Diseases; Vasopressins

In the last decade, cross-sectional and multiple cohort studies have associated total fluid intake or water intake with the risk for chronic kidney disease (CKD) and even the risk of developing hyperglycemia. Urine biomarkers have also been linked to the risk of CKD and lithiasis, and these biomarkers respond quickly to variations in fluid intake. High circulating copeptin levels, a surrogate marker of arginine vasopressin, have been associated with metabolic syndrome, renal dysfunction and increased risk for diabetes mellitus, cardiovascular disease and death. The aim of this paper was to explore how the various findings on water intake, hydration and health are interconnected, to highlight current gaps in our understanding and to propose a model that links water intake, homeostatic mechanisms to maintain water balance and health outcomes. Since plasma copeptin and vasopressin have been demonstrated to be sensitive to changes in water intake, inversely associated with 24-hour urine volume, and associated with urine biomarkers and fluid intake, vasopressin is proposed as the central player in this theoretical physiological model.

Topics: Arginine Vasopressin; Biomarkers; Cardiovascular Diseases; Diabetes Mellitus; Drinking; Glycopeptides; Health Status; Humans; Hyperglycemia; Metabolic Syndrome; Models, Biological; Renal Insufficiency, Chronic; Risk Factors; Vasopressins; Water-Electrolyte Balance

Type 2 diabetes and its cardiovascular disease complications are the major public health threats of our century. Although physical activity and dietary changes are the cornerstones in prevention of diabetes, their broad implementation is not elementary and other complementary lifestyle regimens are needed.. Vasopressin (VP) is the main regulator of body water homeostasis, and at insufficient water intake, normal plasma osmolality can be maintained by increased pituitary VP secretion through VP-2 receptor mediated renal water reabsorption. During the last 6 years several independent studies have shown that high circulating VP, measured by the stable VP marker copeptin, predicts development of type 2 diabetes as well as the metabolic syndrome, cardiovascular disease and premature mortality. Interestingly, VP stimulates adrenocorticotrophic hormone, and as a consequence cortisol secretion, through pituitary VP-1B receptors, which could explain why the 25% of the middle-aged population with high circulating VP have a mild Cushing's syndrome-like phenotype. In rats, high VP results in deterioration of glucose tolerance whereas low VP, obtained by high water intake, ameliorates the VP associated dysmetabolic state, suggesting that the relationship between high VP and risk of diabetes and cardiometabolic disease in humans may be causal and reversible by increasing water intake.. With the emerging evidence that high VP, which is present in 25% of the population, is an independent risk factor for diabetes and cardiometabolic disease, VP reduction through water supplementation appears as an attractive candidate intervention to prevent diabetes and its cardiovascular complications.

Topics: Animals; Cardiovascular Diseases; Diabetes Mellitus, Type 2; Drinking; Glycopeptides; Humans; Metabolic Syndrome; Osmolar Concentration; Pituitary Gland, Posterior; Receptors, Vasopressin; Risk Factors; Vasopressins; Water-Electrolyte Balance

Reliable data at population level are essential to firmly establish links between fluid intake, hydration and health, investigate dose-response relationships and develop meaningful public health strategies or reference intake values. However, limited research exists regarding the most appropriate methodology for assessing beverage or total fluid intake (TFI). To date, methodologies have been developed to assess food and nutrient intake without due consideration of water or fluid intake behavior. A recent crossover study showed that a 24-hour food recall significantly underestimated mean TFI by 382 ml (95% CI 299-465) compared with a fluid specific 7-day record. The authors postulated that this average difference was mainly the result of missed drinking acts between meals a 24-hour recall was used. Using a 7-day record administered in paper form or on-line has also been shown to lead to a significantly different mean TFI of 129 ml. Therefore, the choice of methodology might result in measurement errors that limit between-survey or between-country comparisons. Such errors may contribute to variations in estimates of TFI that cannot be explained by differences in climate, physical activity or cultural habits. A recent survey confirmed the variation in methodologies used in European national dietary surveys. Since these surveys form the basis for setting adequate intakes for total water intake, measurement error between surveys should be limited, highlighting the need for the development of a consistent methodology that is validated for water and TFI estimation.

Topics: Arginine Vasopressin; Biomarkers; Cardiovascular Diseases; Dehydration; Drinking; Female; Glomerular Filtration Rate; Glycopeptides; Health Status; Humans; Hyperglycemia; Male; Metabolic Syndrome; Models, Biological; Prognosis; Renal Insufficiency, Chronic; Risk Factors; Urine; Vasopressins; Water-Electrolyte Balance

Panayiotopoulos syndrome is a benign idiopathic childhood epilepsy characterized by altered autonomic activity at seizure onset.. Three siblings with Panayiotopoulos syndrome underwent 24-hour EEG recording and head-up tilt testing with continuous blood pressure and RR interval monitoring. Plasma catecholamines and vasopressin were measured while supine, upright, and during a typical seizure.. Patient 1, a 12-year-old girl, had a history of involuntary lacrimation, abdominal pain, and recurrent episodes of loss of muscle tone and unresponsiveness followed by somnolence. Her EEG revealed bilateral frontotemporal spikes. Patient 2, a 10-year-old boy, had episodic headaches with pinpoint pupils, skin flushing of the face, trunk, and extremities, purple discoloration of hands and feet, diaphoresis, nausea, and vomiting. Tilt testing triggered a typical seizure after 9 minutes; there was a small increase in blood pressure (+5/4 mm Hg, systolic/diastolic) and pronounced increases in heart rate (+59 bpm) and norepinephrine (+242 pg/mL), epinephrine (+175 pg/mL), and vasopressin (+22.1 pg/mL) plasma concentrations. Serum glucose was elevated (206 mg/dL). His EEG revealed right temporal and parietal spikes. Patient 3, an 8-year-old boy, had a history of restless legs at night, enuresis, night terrors, visual hallucinations, cyclic abdominal pain, and nausea. His EEG showed bitemporal spikes.. Hypertension, tachycardia, and the release of vasopressin suggest activation of the central autonomic network during seizures in familial Panayiotopoulos syndrome. These autonomic and neuroendocrine features may be useful in the diagnosis and may have therapeutic implications.

Topics: Cardiovascular Diseases; Catecholamines; Child; Chromatography, High Pressure Liquid; Electroencephalography; Endocrine System Diseases; Epilepsy, Benign Neonatal; Epilepsy, Rolandic; Female; Humans; Male; Plethysmography; Siblings; Spectrum Analysis; Vasopressins

Several new biomarkers are related to mortality in community-acquired pneumonia (CAP).. Aim of this study was to compare new biomarkers for the prediction of short- and long-term all-cause mortality in CAP.. We enrolled 728 patients (59.0 ± 18.2 yr) with CAP. Midregional proadrenomedullin (MR-proADM), midregional proatrial natriuretic peptide (MR-proANP), proarginin-vasopressin (copeptin), proendothelin-1 (CT-proET-1), procalcitonin (PCT), C-reactive protein, white blood cell (WBC) count, and clinical confusion, respiratory rate, blood pressure, and age over 65 years (CRB-65) score were determined on admission. Patients were followed up for 180 days.. In patients who died of any cause within 28 and 180 days (2.5 and 5.1%, respectively), MR-proADM, MR-proANP, copeptin, CT-proET-1 and PCT as well as CRB-65 were significantly higher compared with survivors. MR-proADM had the best performance for 28 days (HR 3.67) and 180 days (HR 2.84) survival. The C index of MR-proADM for 28-day survival (0.85) was superior to MR-proANP (0.81), copeptin (0.78), CT-proET-1 (0.79), and CRB-65 (0.72) for the prediction of mortality. For prediction of mortality at 180 days, the C index of MR-proADM (0.78) was higher than that for MR-proANP (0.74), copeptin (0.73), CT-proET-1 (0.76), PCT, C-reactive protein, and white blood cells. MR-proADM was independent of CRB-65, and added prognostic information for short- and long-term mortality. MR-proADM was an independent and strong predictor of short- and long-term mortality.. All new biomarkers were good predictors of short- and long-term all-cause mortality, superior to inflammatory markers, and at least comparable to CRB-65 score. MR-proADM showed the best performance. A combination of CRB-65 with MR-proADM might be the best predictor for mortality.

Topics: Adolescent; Adrenomedullin; Adult; Age Distribution; Aged; Aged, 80 and over; Atrial Natriuretic Factor; Biomarkers; Blood Pressure; C-Reactive Protein; Calcitonin; Calcitonin Gene-Related Peptide; Cardiovascular Diseases; Community-Acquired Infections; Comorbidity; Endothelin-1; Female; Germany; Humans; Inflammation; Leukocyte Count; Male; Middle Aged; Pneumonia; Predictive Value of Tests; Protein Precursors; Respiratory Rate; Survival Analysis; Vasopressins; Young Adult

Recent studies have suggested that endogenous vasopressin (AVP) acts as a spasmogen during coronary artery bypass grafting (CABG). Given that AVP could induce vasospasm in the grafted vessel, we assessed the release of this peptide during and after CABG, and explored ways of counteracting its contractile effect on the internal mammary artery (IMA).. Plasma levels of AVP were determined by radioimmunoassay in 16 patients before, during and after CABG. Using isometric force recording techniques, we also investigated the mechanisms involved in the contractile effect of AVP in ring preparations of IMA specimens taken from 95 patients.. Plasma AVP levels peaked after the start of cardiopulmonary bypass (CPB) and correlated well with serum osmolality (Pearson's r=0.9490; P<0.0001; n=16). An inverse correlation was observed between plasma AVP levels recorded at this stage and the maximal contraction induced in vitro by AVP in vascular rings from the same patients (Pearson's r=-0.6968; P<0.01; n=16). No change in the AVP response was produced by endothelium removal, exposure to the NO precursor (3 x 10(-4)M L-arginine), inhibition of nitric oxide (NO) synthase (3 x 10(-5) M L-NAME) or soluble guanylate cyclase (3 x 10(-6) M 1H-[1,2,4]oxadiazol [4,3,-alpha]quinoxalin-1-one (ODQ)), removal of the superoxide anion (100 U/ml superoxide dismutase (SOD) plus 1200 U/ml catalase) or hydroxyl radical (10(-4) M deferoxamine), or specific alpha1 - (10(-6) M prazosin) or endothelin (10(-5) M bosentan) receptor antagonism. In contrast, adenylate cyclase activation (3 x 10(-8) M forskolin) reduced the contractile response to AVP, while prostanoid synthesis (3 x 10(-6) M indomethacin) inhibition and blockade of Ca2+ -activated potassium channels (KCa) (10(-3) M tetraethylammonium (TEA)) enhanced AVP contraction. Age, gender and smoking also modified the AVP response.. Our findings suggest a role for AVP as a modulator of vascular tone in human IMA. The effect of AVP is dependent on prostanoids and Ca2+ -activated K+ channels, so its dysfunction in pathophysiological cardiovascular processes could mean that AVP, among other factors, produces vasospasm in IMA grafts.

Topics: Aged; Cardiovascular Diseases; Dose-Response Relationship, Drug; Female; Humans; Internal Mammary-Coronary Artery Anastomosis; Male; Mammary Arteries; Middle Aged; Osmolar Concentration; Potassium; Potassium Channels, Calcium-Activated; Prostaglandins; Risk Factors; Sodium; Tissue Culture Techniques; Vasoconstriction; Vasopressins

Topics: Cardiovascular Diseases; Humans; Hyponatremia; Vasoconstrictor Agents; Vasopressins

Sleep impairment is one of the major side effects of glucocorticoid therapy. The mechanism responsible for this circadian disorder is unknown, but alterations in the suprachiasmatic nucleus (SCN), the biological clock of the human brain, are presumed to play a major role. In the present study, the amount of vasopressin mRNA (AVP mRNA) expression in the SCN was investigated in 10 glucocorticoid-exposed patients and 10 glucocorticoid free, age- and clock time of death-matched controls. The total amount of AVP mRNA, expressed as masked silver grains in the SCN, was two times lower in glucocorticoid-exposed patients (n = 10; 5115 +/- 1314 microm(2)) than that in controls (n = 10; 11,021 +/- 1408 microm(2)) (P = 0.006). There was also a 53% decrease in the total number of profiles in the SCN that expressed AVP mRNA in glucocorticoid-exposed patients (16,759 +/- 3110) compared with those in controls (31,490 +/- 3816) (P = 0.01). In conclusion, glucocorticoids have an inhibitory effect on AVP mRNA expression in the human SCN, which may be the biological basis of the circadian rhythm disturbances during glucocorticoid therapy.

Topics: Adult; Aged; Autopsy; Cardiovascular Diseases; Female; Gene Expression; Glucocorticoids; Humans; Male; Middle Aged; Neoplasms; RNA, Messenger; Suprachiasmatic Nucleus; Vasopressins

A group of 41-year-old hypertensive men (n = 35, blood pressure (BP) 149.9 +/- 2.1/98.9 +/- 1.1 mmHg, mean +/- SEM) who had never received treatment for their condition were compared with hypertensive women of the same age (n = 18, BP 155.9 +/- 4.3/98.1 +/- 1.6 mmHg) with comparable body mass index (BMI, 25.9 +/- 0.5 vs. 24.9 +/- 4.5 kg m-2) who, also, had never received treatment. The lipid profile was more atherogenic in the men, with lower HDL cholesterol (1.21 +/- 0.04 vs. 1.38 +/- 0.06 mmol l-1, P = 0.04), higher total cholesterol (6.04 +/- 0.14 vs. 5.54 +/- 0.18 mmol l-1, P = 0.04) and triglycerides (1.80 +/- 0.16 vs. 0.96 +/- 0.10 mmol l-1, P < 0.001). The hypertensive men had higher haemoglobin (P < 0.001) and haematocrit. Plasma catecholamines were inversely related to BMI in the women only (r = -0.52, P < 0.05 for both noradrenaline and adrenaline). Women with BMI above 25 kg m-2 had significantly lower arterial plasma adrenaline and noradrenaline than those with BMI below 25 kg m-2 (28 +/- 5 vs. 78 +/- 16 pg ml-1, P < 0.01 and 101 +/- 17 vs. 206 +/- 33 pg ml-1, P < 0.01 respectively). A negative curvilinear relationship appeared between arterial adrenaline and insulin (r = 0.49, P = 0.05). These results suggest a male propensity for athero-thrombogenic risk factors in otherwise comparable hypertensive subjects. A close relationship between metabolic risk factors within the normal range seems to exist even in hypertensive women. The decreased sympathetic activity at rest in the obese hypertensive women indicates different pathophysiological mechanism for hypertension in lean and obese. Decreased sympathetic activity and thus reduced energy expenditure, promotes a risk for weight gain, and could explain the inverse relationship between insulin and adrenaline.

Topics: Adult; Body Mass Index; Cardiovascular Diseases; Catecholamines; Electrolytes; Female; Hematocrit; Hemoglobins; Humans; Hypertension; Insulin; Lipids; Male; Renin; Risk Factors; Sex Characteristics; Vasopressins

Vasopressin has been used for 25 years to control bleeding from esophageal varices. Its efficacy is believed to be due to a direct vasoconstrictor activity on splanchnic arterioles and precapillary sphincters, with secondary reduction in portal venous blood flow and pressure. While it has been administered by both the intra-arterial and intravenous routes, the latter has gained favor in the light of laboratory and clinical investigations. The most common complications are cardiovascular, and bradycardia is an early sign of toxicity; adverse effects may be avoided with simultaneous infusion of isoproterenol. Vasopressin has not been shown to prolong survival from esophageal bleeding. It is effective in controlling upper gastrointestinal hemorrhage and is commonly viewed as a means of buying time to prepare the patient for shunt surgery. Vasopressin infusion may reduce both operation time and blood loss during shunt surgery. New analogs of vasopressin presently under investigation may facilitate its administration and reduce morbidity.

Topics: Cardiovascular Diseases; Esophageal and Gastric Varices; Gastrointestinal Hemorrhage; Humans; Infusions, Intra-Arterial; Infusions, Parenteral; Splanchnic Circulation; Vasopressins

Topics: Animals; Blood Pressure; Cardiovascular Diseases; Dogs; Heart; Humans; Kidney; Lung; Pressoreceptors; Reflex; Renal Circulation; Renin; Vasopressins

Topics: Adult; Aged; Aging; Animals; Cardiovascular Diseases; Coronary Vessels; Dogs; Heart; Hemodynamics; Homeostasis; Humans; Hypothalamo-Hypophyseal System; Middle Aged; Rabbits; Rats; Vasopressins

Topics: Adult; Aged; Aging; Animals; Arrhythmias, Cardiac; Cardiovascular Diseases; Cerebrovascular Disorders; Coronary Disease; Humans; Hypertension; Middle Aged; Rabbits; Rats; Vasopressins

Topics: Acridines; Angiotensin II; Animals; Blood Pressure; Caffeine; Cardiovascular Diseases; Cardiovascular System; Dog Diseases; Dogs; Epinephrine; Norepinephrine; Octopamine; Peristalsis; Theophylline; Vasopressins

Topics: Adult; Anesthesia, Dental; Anesthesia, Local; Blood Pressure; Cardiovascular Diseases; Diazepam; Electrocardiography; Epinephrine; Felypressin; Female; Heart Rate; Humans; Male; Middle Aged; Vasoconstrictor Agents; Vasopressins

Topics: Adolescent; Adult; Aged; Biopsy; Cardiovascular Diseases; Female; Hemostatics; Humans; Middle Aged; Uterine Cervical Neoplasms; Vaginal Smears; Vasopressins

Topics: Aged; Blood Volume Determination; Cardiovascular Diseases; Cerebrovascular Disorders; Chromium Isotopes; Gastrointestinal Diseases; Gastrointestinal Hemorrhage; Hematocrit; Hemoglobinometry; Humans; Hydrocortisone; Iodine Isotopes; Metaraminol; Methylphenidate; Phenoxybenzamine; Respiratory Tract Diseases; Shock, Hemorrhagic; Urologic Diseases; Vasopressins

Topics: Aldosterone; Blood Circulation; Blood Volume; Cardiovascular Diseases; Heart Failure; Humans; Kidney; Physiology; Sodium; Vasopressins; Water

Topics: Cardiovascular Diseases; Heart; Humans; Myocardial Infarction; Pituitary Gland; Pituitary Hormones; Vasopressins

Topics: Androgens; Atropine; Cardiovascular Diseases; Heart; Infarction; Myocardial Infarction; Pituitary Diseases; Pituitary Gland; Pituitary Hormones; Testosterone; Vasopressins