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)

Vasopressin, like all the other neuro-hormonal systems, is activated in patients with cardiac insufficiency. Vasopressin attaches itself to two distinct specific receptors. It is through the intermediary of the renal V2 receptor, controlling the reabsorption of water by the collecting duct, that vasopressin finely regulates the blood osmolarity. The ubiquitous V1a receptor is essentially responsible for the vasoconstrictor effect of the hormone. Some specific antagonists for these two receptors have now been evaluated in various pathologies such as SIADH, cirrhosis or cardiac insufficiency. In this situation the mixed antagonists, anti-V1a-V2, seem more appropriate than the specific V1a or V2 receptor antagonists. The results of the first human studies are encouraging. The mixed antagonists reduce the pulmonary capillary pressure and increase diuresis and clearance of free water. But further studies are necessary to confirm these results and to demonstrate a reduction in morbidity and mortality before adding this class of medication to the therapeutic arsenal for our patients with cardiac insufficiency.
Arch Mal Coeur Vaiss 2002 Feb
PMID:[Vasopressin antagonists]. 1193 60

Regarding cardiac failure, the year 2004 was notable for the dissemination of indications for the use of medical devices in heart failure: indications for cardioversion with the long awaited publication of the COMPANION study, advancement of the concept of intra-ventricular asynchronism, and studies of defibrillators in non-ischaemic cardiac failure (COMPANION, DEFINITE, SCD-HeFT, TOVA). Furthermore, pragmatic clinical studies allowed refinement of the uses of BNP (diagnostic and prognostic), underlining the importance of renal function and its progression during hospitalisation, and the risks of using strong, modern therapy in populations without "ad hoc" surveillance which do not correspond with study populations (aldactone in Canada). Just as in coronary patients, it appears to be important to commence full medical treatment prior to hospital discharge, because treatment is rarely changed thereafter. The management of seriously ill patients is evolving with several therapeutic advances: the methods of selecting patients for heart transplants have changed, with the advancement of opportunities for circulatory assistance. Attention has also been turned to the significant group, still poorly understood, of patients with diastolic heart failure, for whom diagnostic methods have been defined, as well as their clinical characteristics. Lastly the medication studies: new drugs in acute cardiac failure (preliminary results for vasopressin antagonists), wider indications for betablockers in elderly subjects (SENIORS), and advances in cellular cardiomyoplasty (using haemopoietic stem cells especially this year). It has been a fruitful year, difficult to summarise in a few lines, or even several pages....
Arch Mal Coeur Vaiss 2005 Jan
PMID:[The best of cardiac failure in 2004]. 1571 60

Hyponatraemia is a common clinical finding in cardiac failure, complicating the management of these patients. Vasopressin plays a fundamental role in the physiopathology of the hyponatraemia of cardiac failure and binds to two distinct specific receptors, receptor V1a and V2. The V2 receptors, situated in the renal collecting duct, control the resorbtion of free water. The V1a receptors, present everywhere, are responsible for the vasoconstrictive effect of vasopressin. Specific antagonists of vasopressin receptors are being evaluated in pathologies associated with hyponatraemia. The preliminary results in patients with cardiac failure are encouraging and mortality studies are underway.
Arch Mal Coeur Vaiss 2006 Mar
PMID:[Hyponatraemia, antagonists of the antidiuretic hormone and cardiac failure]. 1661 24

Desmopressin is a synthetic vasopressin analog that increases the plasma levels of coagulation factor VIII, von Willebrand factor, and tissue plasminogen activator. This hemostatic agent, which can be administered either parenterally or intranasally, has been approved for use in the prevention and treatment of hemorrhagic events during surgery in patients with hemophilia A, in cases of prolonged idiopathic bleeding, and for complications associated with platelet antiaggregant therapy. This case report describes cardiac toxicity associated with desmopressin administered according to the recommended indications: a 55-year-old woman diagnosed with Wegener's granulomatosis (WG) was treated with desmopressin to improve hemostasis and shorten bleeding time before a planned renal biopsy. She developed cardiac arrest within 60 minutes of the desmopressin injection. Cardiopulmonary resuscitation began immediately and was successful, although the patient subsequently died of WG-associated complications. Desmopressin administration thus appears, in some cases, to be associated with a high risk of thrombotic events, possibly by stimulating the rapid release of endothelial factors such as an abnormal multimeric form of von Willebrand factor, which might cause platelet aggregation. Clinicians should be aware of the possible occurrence of this little-known but potentially serious cardiac event associated with desmopressin administration and be prepared to initiate cardiopulmonary resuscitation immediately if needed.
J Mal Vasc 2013 Feb
PMID:Desmopressin-related myocardial infarction in a patient with Wegener's granulomatosis: a case report and review of the literature. 2326 78


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