Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Disorders of body fluids are among the most commonly encountered problems in the practice of clinical medicine. This is in large part because many different disease states can potentially disrupt the finely balanced mechanisms that control the intake and output of water and solute. It therefore behoves clinicians treating such patients to have a good understanding of the pathophysiology, the differential diagnosis and the management of these disorders. Because body water is the primary determinant of the osmolality of the extracellular fluid, disorders of body water homeostasis can be divided into hypo-osmolar disorders, in which there is an excess of body water relative to body solute, and hyperosmolar disorders, in which there is a deficiency of body water relative to body solute. The classical hyperosmolar disorder is diabetes insipidus (DI), and the classical hypo-osmolar disorder is the syndrome of inappropriate antidiuretic hormone secretion (SIADH). This chapter first reviews the regulatory mechanisms underlying water and sodium metabolism, the two major determinants of body fluid homeostasis. The major disorders of water metabolism causing hyperosmolality and hypo-osmolality, DI and SIADH, are then discussed in detail, including the pathogenesis, differential diagnosis and treatment of these disorders.
Best Pract Res Clin Endocrinol Metab 2003 Dec
PMID:Disorders of body water homeostasis. 1468 85

Refractory ascites indicates advanced chronic liver disease and represents a therapeutic challenge. It may be triggered by spontaneous bacterial peritonitis and denotes poor prognosis. While liver transplantation is the ultimate treatment, for the relief of ascites therapeutic paracentesis with iv-administration of albumin and/or transjugular intrahepatic portosystemic shunt (TIPS) are well established. With rapid deterioration of renal function patients can develop hepatorenal syndrome. There is increasing evidence that these patients can be bridged to transplantation with vasopressin analogs (terlipressin) and albumin.
Best Pract Res Clin Gastroenterol 2007
PMID:The patient with refractory ascites. 1754 17

Variceal bleeding is one of the most severe complications of portal hypertension related to liver cirrhosis. Primary prophylaxis is considered mandatory in patients with cirrhosis and high-risk oesophageal varices, and once varices have bled, every effort should be made to arrest the haemorrhage and prevent further bleeding episodes. In acute variceal bleeding, vasoactive drugs that lower portal pressure should be started even before endoscopy, and should be maintained for up to 5 days. The choice of vasoactive drug should be made according to local resources. Terlipressin, somatostatin and octreotide can be used; vasopressin plus transdermal nitroglycerin may be used if no other drug is available. In variceal bleeding, antibiotic therapy is also mandatory. In primary and secondary prophylaxis, beta-blockers are the mainstay of therapy. In secondary prophylaxis (but not in primary prophylaxis) these drugs can be combined with organic nitrates.
Best Pract Res Clin Gastroenterol 2008
PMID:Acute variceal bleeding: pharmacological treatment and primary/secondary prophylaxis. 1834 84

Arginine vasopressin, a hypothalamic peptide hormone, has multiple physiological functions, including body water regulation, control of blood pressure and effects on body temperature, insulin release, corticotropin release, memory and social behaviour. These functions are achieved via at least three specific G-protein-coupled vasopressin receptors. Development of specific vasopressin receptor antagonists in recent years is helping to elucidate the precise actions of vasopressin at each of these receptor types. The complex signalling and messenger processes which take place after receptor stimulation are now more clearly understood. Vasopressin dysregulation can occur in various disease processes, and a better understanding of the mechanisms underlying physiological synthesis, release and regulation of vasopressin will help in the development of therapies to treat these conditions.
Best Pract Res Clin Anaesthesiol 2008 Jun
PMID:Physiology and pathophysiology of the vasopressinergic system. 1868 71

This review article summarizes the structure, signalling pathways, and tissue distribution of the vasopressin receptors, V1 vascular, V2 renal, V3 pituitary, and oxytocin receptors, as well as the P2 class of purinoceptors. The physiological effects of vasopressin on its receptors are described. The future direction with regard to the role of the V1a receptor in circulatory shock states is discussed; further studies with V1a receptor agonists are warranted to further develop treatment strategies to reduce mortality in life threatening diseases like septic shock.
Best Pract Res Clin Anaesthesiol 2008 Jun
PMID:Physiology of the vasopressin receptors. 1868 72

Vasopressin, also called antidiuretic hormone, is a 9 amino-acid peptide, synthesized from a precursor containing neurophysin II, by neurones from the supra-optic and peri-ventricular nuclei, and then stored in the posterior hypophysis. Vasopressin regulates plasmatic osmolality and volaemia via V2 receptors at the levels of the kidney, and vascular smooth muscle tone via V1a arterial receptors. Both its synthesis and release from hypophysis vesicles depend on variations in plasma osmolality, volaemia, and arterial blood pressure. In addition, vasopressin interacts with the main hormonal systems involved in the response to stress, including the hypothalamic-pituitary adrenal axis, other anterior pituitary hormones, mainly prolactin and growth hormone, the renin-angiotensin system, and regulates insulin synthesis and glucose metabolism. Interestingly, during critical illness, exogenous administration of vasopressin showed little effects on the circulating levels of these various hormones, except an increase in prolactin. The absence of endocrine effects of vasopressin during critical illness is unclear and may relate to an already maximal hormonal stimulation or to down-regulation of vasopressin receptors.
Best Pract Res Clin Anaesthesiol 2008 Jun
PMID:Endocrine effects of vasopressin in critically ill patients. 1868 73

Vasodilatory septic shock is characterized by profound vasodilation of the peripheral circulation, relative refractoriness to catecholamines and a relative deficiency of the posterior pituitary hormone, vasopressin. Arginine vasopressin is effective in restoring vascular tone in vasodilatory septic shock and may be associated with decreased mortality in less severe septic shock as well as improved mortality and decreased renal failure in septic shock patients at risk for renal failure.
Best Pract Res Clin Anaesthesiol 2008 Jun
PMID:Arginine vasopressin in the treatment of vasodilatory septic shock. 1868 74

Given the controversial experimental and clinical data reported in the literature, up to now it is rather difficult to draw a definitive conclusion on the effects of V1 agonists on splanchnic haemodynamics. Nevertheless, it must be underscored that most of the experimental studies assessing the effects of low dose V1 agonist infusion in hyperdynamic models did not demonstrate any detrimental effect on splanchnic haemodynamics both at macro- and microcirculatory levels. Interestingly, all the reported studies focused on macro- and microcirculatory haemodynamics, while only some also addressed the local oxygenation and metabolism. In clinical studies in patients with septic shock, data are accumulating regarding the absence of clinically relevant side effects in the splanchnic region when vasopressin is used, but conversely little is known about the safety of terlipressin, mainly because of the small number of patients studied. Thus, the absence of clinically harmful effect does not exclude covert splanchnic ischaemia, which may counterbalance the beneficial systemic effects.
Best Pract Res Clin Anaesthesiol 2008 Jun
PMID:Impact of vasopressin analogues on the gut mucosal microcirculation. 1868 80

The synthetic vasopressin analogue, terlipressin, is being increasingly used to treat catecholamine-resistant hypotension in septic shock and other conditions. While terlipressin holds some theoretical and anecdotal advantages over vasopressin, this has not been formally tested in prospective randomised trials. This review analyses the published literature and makes comparisons, where possible, between vasopressin and terlipressin.
Best Pract Res Clin Anaesthesiol 2008 Jun
PMID:Arginine vasopressin vs. terlipressin in the treatment of shock states. 1868 81

Vasopressin analogues are increasingly used for haemodynamic support of catecholamine-refractory, hyperdynamic septic shock. Arginine vasopressin (AVP) and terlipressin (TP) effectively increase mean arterial pressure and reduce catecholamine requirements in this condition. However, the use of either of the drugs may be linked to relevant haemodynamic side effects, including reductions in cardiac output, oxygen delivery and mixed-venous oxygen saturation. These alterations may result in impaired tissue perfusion and foster the genesis of ischemic tissue injury. In addition, decreases in platelet count and increases in aminotransferases activity and bilirubin concentration have been reported with the use of V1 agonists. However, it remains unclear whether these changes are of clinical relevance. This review article summarizes the previous data on adverse effects related to the therapy with vasopressin analogues and discusses potential options to prevent such adverse events. In summary, continuous TP infusion appears to be superior to bolus infusion. Maximum doses of 0.03 (-0.067) U min(-1) of AVP or 2 microg kg(-1) h(-1) of TP, respectively, should not be exceeded. Aggressive fluid therapy may prevent adverse haemodynamic effects linked to infusion of either AVP or TP. Finally, platelet count, surrogate variables of hepatic dysfunction, electrolytes and osmolality should be strictly monitored in patients treated with vasopressin analogues.
Best Pract Res Clin Anaesthesiol 2008 Jun
PMID:Vasopressin analogues in the treatment of shock states: potential pitfalls. 1868 84


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