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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Portal hypertension is a common complication of hepatic cirrhosis, and is responsible for much of the mortality and morbidity associated with advanced liver disease. Esophageal varices are a common occurrence, and esophageal variceal hemorrhage carries a high mortality. Endoscopic therapies have proven effective in treating active bleeding and preventing recurrence, but several pharmacological agents are useful adjuncts to endoscopy in both acute bleeding and in the primary and secondary prophylaxis of variceal hemorrhage. In acute hemorrhage, vasoconstricting agents such as vasopressin, terlipressin, somatostatin, and octreotide have been demonstrated to add benefit to endoscopic therapy. Secondary prophylaxis includes endoscopic therapy to eradicate varices, usually combined with oral beta-blockers. Primary prophylaxis is typically used in patients with medium or large varices, and consists of oral beta-blockers, at times combined with oral nitrates. This paper the reviews the pharmacological principles behind these therapies, and the clinical trial data that has led to their widespread use.
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PMID:Pharmacological therapy for the treatment of esophageal varices. 1655 91

Diabetes insipidus in pregnancy has different causes. The association of diabetes insipidus with disturbances of liver function has been reported, however, diabetes insipidus has rarely been reported in HELLP syndrome. We present a 23-year-old primigravida with a singleton gestation complicated by HELLP syndrome who developed postpartum diabetes insipidus. Labor was induced promptly to terminate pregnancy because of intrauterine fetal death and liver dysfunction. 1-deamino-8-D-arginine-vasopressin was administered. Diabetes insipidus and liver dysfunction resolved within 2 weeks. Development of diabetes insipidus may result from increased vasopressinase activity mainly caused by deterioration of liver functions caused by HELLP syndrome. In pregnant women with liver disease as a result of any cause, the development of diabetes insipidus should be assessed with particular attention.
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PMID:Transient postpartum diabetes insipidus associated with HELLP syndrome. 1710 Aug 23

Accumulation of fluid as ascites is the most common complication of cirrhosis. This is occurring in about 50% of patients within 10 years of the diagnosis of cirrhosis. It is a prognostic sign with 1-year and 5-year survival of 85% and 56%, respectively. The most acceptable theory for ascites formation is peripheral arterial vasodilation leading to underfilling of circulatory volume. This triggers the baroreceptor-mediated activation of renin-angiotensin-aldosterone system, sympathetic nervous system and nonosmotic release of vasopressin to restore circulatory integrity. The result is an avid sodium and water retention, identified as a preascitic state. This condition will evolve in overt fluid retention and ascites, as the liver disease progresses. Once ascites is present, most therapeutic modalities are directed on maintaining negative sodium balance, including salt restriction, bed rest and diuretics. Paracentesis and albumin infusion is applied to tense ascites. Transjugular intrahepatic portosystemic shunt is considered for refractory ascites. With worsening of liver disease, fluid retention is associated with other complications; such as spontaneous bacterial peritonitis. This is a primary infection of ascitic fluid caused by organisms originating from large intestinal normal flora. Diagnostic paracentesis and antibiotic therapy plus prophylactic regimen are mandatory. Hepatorenal syndrome is a state of functional renal failure in the setting of low cardiac output and impaired renal perfusion. Its management is based on drugs that restore normal renal blood flow through peripheral arterial and splanchnic vasoconstriction, renal vasodilation and/or plasma volume expansion. However, the definitive treatment is liver transplantation.
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PMID:Fluid retention in cirrhosis: pathophysiology and management. 1818 68

Hepato-renal syndrome (HRS) is a functional renal failure complicating end-stage liver disease. HRS is characterized by marked arterial vasodilation (mainly of the splanchnic bed) and severe renal vasoconstriction. HRS is classified into 2 types: type I HRS shows a rapid and progressive decline in renal function with a very poor prognosis (median survival of about 2 weeks); HRS type 2 has a more stable renal failure, with a median survival of about 6 months. The management of HRS is still a big challenge. The definitive therapy for HRS is liver transplantation (LT); however, the survival rate of HRS patients is poor, and important organ shortage exists. Various approaches have been used for HRS treatment including vasoconstrictor therapy. Recent evidence has shown that vasoconstrictor agents are effective and serve as a bridge to LT; the rationale for vasoconstrictors is to counteract the splanchnic arterial vasodilation and increase the effective arterial blood volume. Thus, renal perfusion and glomerular filtration rates improve. Terlipressin, a V1 vasopressin agonist, has been used frequently. A recent meta-analysis of clinical trials showed that the pooled rate of patients who reversed HRS after terlipressin therapy was 0.52 (95% CI, 0.42; 0.61; P = 0.0001, /2 = 24.6%). The pooled Odds Ratio (OR) for mortality rate in HRS patients who were not responders to terlipressin versus responders was 5.746 (95% CI, 1.5; 21.9; P = 0.0005). Prospective, controlled clinical trials are in progress to address the impact of vasoconstrictor use on survival in HRS patients. Alternative therapies such as transjugular intrahepatic portosystemic shunts (TIPS) and extracorporeal albumin dialysis (ECAD) have given encouraging results but experience is extremely limited.
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PMID:Recent advances in the management of hepato-renal syndrome (HRS). 1828 7

Hepatorenal syndrome is a form of acute or sub-acute renal failure which develops in patients with chronic liver disease. In contrast to other forms of acute renal failure it may be reversible using pharmacological agents. The pathogenesis involves splanchnic vasodilatation and intense renal vasoconstriction. Increasing intravascular volume and prolonged treatment with vasoconstrictor drugs reverses renal failure in a significant proportion of patients. Agents currently used include the vasopressin analogues terlipressin and the alpha1-adrenoceptor agonist midodrine. The somatostatin analogue octreotide has been used in combination therapy but is ineffective as monotherapy. Intravenous albumin is an important adjunctive treatment both in the prevention and treatment of hepatorenal syndrome. Increasing intravascular volume using TIPS (transjugular intrahepatic stent shunt) is effective in some patients and may be useful in maintaining patients who have initially responded to pharmacological therapy. Despite improvements in survival, long term prognosis is still poor and generally depends on the degree of reversibility of the underlying liver disease or access to liver transplantation.
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PMID:Management of hepatorenal syndrome. 1853 34

Arginine vasopressin is a naturally occurring peptide with established physiological functions acting as a vasoconstrictor through V1 receptors or an aquagenic agent allowing free water retention through V2 receptors in the kidney. Portal haemodynamic changes of chronic liver disease are responsible for the lethal consequences of cirrhosis--bleeding oesophageal varices and hepatorenal syndrome. Increasing hepatic vascular resistance to blood flow coupled with central hypovolaemia and a hyperdynamic circulation driven by changes in nitric oxide responsiveness disturbs the normal circulatory physiology raising portal pressure. Vasopressin and its analogues are potent vasoconstrictors and can be utilised in the management of the complications of cirrhosis. Hyponatraemia is common in end stage liver disease due in part to sodium retention and a decreased free water clearance. Diuretic therapy often leads to a worsening of the sodium status and have little true effect on improving free water clearance. Recently a new class of drugs, V2 receptor antagonists, have been evaluated in chronic liver disease whereby increasing free water clearance they may reduce ascitic fluid development. This review addresses the pharmacology of both vasopressin agonists and antagonists, their clinical application and future potential roles in managing patients with acute on chronic liver failure.
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PMID:Vasopressin in liver disease--should we turn on or off? 1878 2

Portal hypertension is associated with splanchnic vasodilation which is claimed responsible for the maintenance of chronically elevated portal pressure. Vasopressin analogues are used in the treatment of acute variceal bleeding, since they effectively reduce splanchnic blood flow and portal pressure. Dehydration stimulates the release of endogenous vasopressin release. Here we compared the effects of deprivation of drinking water for 18 h with those of vasopressin infusion on mesenteric hemodynamics in portal vein-ligated (PVL) and sham-operated (SHAM) rats. Blood flow in the superior mesenteric artery was measured with the ultrasonic transit time shift technique. Deprivation of drinking water had no hemodynamic effects in SHAM rats, but completely reversed the mesenteric hyperemia and portal hypertension in PVL rats to figures measured in SHAM rats, without altering blood pressure. Similarly, intravenous infusion of low doses of arginine vasopressin (1-10 pmol/min) selectively reduced mesenteric blood flow in PVL rats but had little effect in SHAM rats. These data suggest that control of water balance or aquaretic drugs might have beneficial effects on splanchnic hemodynamics and portal pressure in advanced liver disease, possibly by stimulating endogenous vasopressin release.
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PMID:Restriction of drinking water abrogates splanchnic vasodilation and portal hypertension in portal vein-ligated rats. 1898 88

Terlipressin, a vasopressin agonist, is a commonly used drug with different indications, particularly in patients with end-stage liver disease. As a V(1) receptor agonist, it increases systemic vascular resistance, particularly in the splanchnic area, resulting in a decrease of portal pressure. Besides the approved use for variceal bleeding, terlipressin also has beneficial effects in the treatment of hepatorenal syndrome and norepinephrine-resistant septic shock. In patients with cirrhosis and variceal bleeding, the use of terlipressin reduces the portal vein pressure and decreases the pressure in esophageal varices. This can save lives when skilled endoscopists are not immediately available. Hepatorenal syndrome is associated with vasodilation in the mesenteric circulation with arterial underfilling and consecutive renal vasoconstriction. Restoration of an effective arterial blood volume can be achieved by the combination of terlipressin and volume expansion. In some cases, a success rate of up to 75% is reported. The early use of terlipressin in catecholamine-resistant shock can improve organ perfusion.
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PMID:Pharmacology, clinical efficacy and safety of terlipressin in esophageal varices bleeding, septic shock and hepatorenal syndrome. 1907 11

Both liver and kidney dysfunction are associated with adverse outcomes in critical illness. Advanced liver disease can be complicated by the hepatorenal syndrome (HRS) with liver transplantation offering the best long-term outcome. However, until recently, HRS was associated with such a poor prognosis that this group of patients rarely survived long enough for transplantation to be considered. The use of vasopressin analogues and albumin infusions has improved the management of HRS and outcomes in terms of renal recovery and survival.
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PMID:The liver and kidney in critically ill patients. 1959 Jan 79

Acute deterioration in kidney function often occurs in patients with acute and chronic liver disease admitted to hospital. The true incidence of acute kidney injury (AKI) is unknown due to the difficulty in accurately measuring kidney function in patients with liver failure, and the lack of a consensus definition of AKI. There is a current consensus definition of hepatorenal syndrome (HRS), but in current clinical practice, volume-unresponsive AKI or acute tubular necrosis are much more common causes of AKI in patients with liver disease. Due to arterial vasodilatation and compensatory neuroendocrine activation, these patients are more prone to AKI due to a combination of changes in renal autoregulation and a sudden reduction in effective plasma volume or hypotension. The key management strategy is to prevent the development of HRS, by avoiding nephrotoxins, and preventing infective complications, and maintaining an effective circulating volume. In patients with HRS, treatment centres around daily plasma volume expansion, typically with albumin, in combination with vasopressors, typically vasopressin analogues, such as terlipressin, or noradrenaline. If renal function does not recover, then renal support with dialysis may be appropriate.
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PMID:Management of acute kidney injury in liver disease. 2042 70


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