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)

The mechanism of facilitatory action of vasopressin on memory processes, dependent probably on different neurotransmitter systems, remains unclear. We decided to study the interactions between arginine-vasopressin and ionotropic NMDA receptor. We estimated the influence of various antagonists of NMDA receptor on beneficial effect of arginine-vasopressin on consolidation of conditioned avoidance responses and on retrieval of memory in passive avoidance situation. We have shown that effect of vasopressin on consolidation is significantly reduced by noncompetitive antagonist of ion channel in the NMDA receptor--dizocilpine (MK-801) and competitive antagonist of glycine recognization site--HA-966. Distinctly, effect of the peptide on retrieval is decreased by competitive antagonist of glutamate recognition site--AP-7, competitive antagonist of polyamines site-arcaine and noncompetitive antagonist--MK-801. This suggests that NMDA receptor may participate in the action of vasopressin on memory, but it plays different roles in consolidation and retrieval processes.
Pol J Pharmacol
PMID:Role of NMDA receptor in the effects of arginine-vasopressin on memory processes. 966 33

We predict some essential interactions between the V2 vasopressin renal receptor (V2R) and its selective peptide antagonist desGly9-[Mca1,D-Ile2,Ile4]AVP, and compare these predictions with the earlier ones for the non-peptide OPC-36120 antagonist- and the [Arg8]vasopressin (AVP) agonist-V2 receptor interactions. V2R controls antidiuresis in mammals and belongs to the superfamily of the heptahelical transmembrane (7TM) G protein-coupled receptors (GPCR)s. V2R was built, the ligands docked and the structures relaxed using advanced molecular modeling techniques. Both the agonist and the antagonists (no matter whether of peptide- or non-peptide type) appear to prefer a common V2R compartment for docking. The receptor amino-acid residues, potentially important in ligand binding, are mainly in the TM3-TM7 helices. A few of these residues are invariant for the whole GPCR superfamily while most of them are conserved in the subfamily of neurohypophyseal receptors, to which V2R belongs. Some of the equivalent residues in a related V1a receptor have been earlier reported as critical for the ligand affinity.
Acta Biochim Pol 1998
PMID:Molecular modelling of the vasopressin V2 receptor/antagonist interactions. 970 92

The aim of this study has been to investigate the effects of vasopressin and oxytocin on antidepressive and memory improving effects of venlafaxine. Male Wistar rats weighing 180-200 g were used in the study. Venlafaxine (20 mg/kg) was administered po 30 min before the test once, and for 7 and 14 days in the chronic experiments. Oxytocin (1 microg/kg) ip and vasopressin (1 microg/kg) sc were administered only once on the test day, 60 min before the tests. The animals were subjected to Porsolt's test for testing antidepressant activity, and their memory functions (working and spatial memory) were evaluated in the maze test and Morris Water Maze test. Antidepressant effects of venlafaxine could be observed already after single drug administration and the effect was maintained during 7 days of drug administration. Oxytocin also exhibited antidepressant activity, and concurrent administration of venlafaxine and oxytocin helped to maintain antidepressant activity of venlafaxine. Vasopressin was devoid of antidepressant action, yet concurrent administration of vasopressin and venlafaxine did not suppress antidepressant activity of the latter. In the chronic experiment, there was no shortening of passive swimming time. Venlafaxine improved memory in the labyrinth test and in the spatial memory test, whereas oxytocin did not affect memory of the tested animals. Joint administration of venlafaxine and oxytocin did not produce memory improving effect observed after administration of venlafaxine only. Vasopressin improved memory and joint administration of venlafaxine and vasopressin maintained the memory improving effect induced by vasopressin. The regulatory role of neuropeptides and new antidepressant drugs, e.g. venlafaxine in mood status and memory functions may depend on the interactions between monoaminergic and neuropeptidergic systems.
Pol J Pharmacol
PMID:Role of neuropeptides in antidepressant and memory improving effects of venlafaxine. 1286 15

Vasovagal syncope is defined as a reflex loss of consciousness related to reaction to various stimuli as orthostatic stress, pain or emotions connected with loss of muscle postural tone. The aetiology of this disorder is still unknown. The imbalance between the parts of autonomic nervous system and other homeostasis-related systems as renin-angiotensin-aldosterone system, peptides as endothelin, neuropeptide Y, vasopressin, adrenomedullin and cAMP, adenosine and AMP can play an important role in the development of vasovagal syncope. In the first part of the paper the authors describe the mechanisms involved in the development of vasovagal reaction, pathophysiology of the head-up tilt test and the role of autonomic nervous system.
Pol Merkur Lekarski 2003 Apr
PMID:[Neurohumoral mechanisms for vasovagal syncopes. Part I]. 1286 5

The inhibitory effect of lipopolysaccharides (LPS) on alpha-adrenergic contraction is quite well known, but molecular mechanism of this inhibition is unclear. In the present study, the interaction between alpha-adrenoceptor and vasopressin receptor response, and LPS in rat tail artery was investigated using chemical stimulation. In the presence of LPS, noradrenaline, phenylephrine and arginine-vasopressin, concentration-response curves (CRCs) were shifted to the right with the change in maximal responses. The K(A) and K(B) values calculated in the presence and absence of LPS did not differ significantly. The results strongly suggest that LPS did not change the receptors affinity. The changes in the relationship between receptor occupancy and response to an agonist in the presence of LPS and reduction of K(A)/ED(50) value suggest reduction of receptor reserve. In the presence of angiotensin II (Ang II), CRCs were shifted to the right with significant increase in receptor reserve. Moreover, this effect was still present in LPS-pretreated arteries. The receptor reserve reduced by LPS significantly increased in the presence of Ang II. It suggests that inhibitory effect of LPS is partially reversible. The results strongly suggest that in early endotoxemia, inhibitory effect of LPS may by partially reverted by an increase in activity of renin-angiotensin-aldosterone system.
Pol J Pharmacol
PMID:Physiological antagonism of angiotensin II and lipopolysaccharides in early endotoxemia: pharmacometric analysis. 1470 72

In recent years, a massive effort has been directed towards designing potent and selective antagonists of neurohypophyseal hormones substituted at position 3. Modification of vasopressin at position 3 with 4,4'-biphenylalanine results in pharmacologically inactive analogues. Chemically, this substitution appears to vary only slightly from those previously made by us (1-Nal or 2-Nal), which afforded potent agonists of V(2) receptors. In this situation, it seemed worthwhile to study the structure of the analogues with 4,4'-biphenylalanine (BPhe) at position 3 in aqueous solution using NMR spectroscopy and total conformational analysis. This contribution is part of extensive studies aimed at understanding spatial structures of 3-substituted [Arg(8)]vasopressin analogues of different pharmacological properties. NMR data were used to calculate 3D structures for all the analogues using two methods, EDMC with the ECEPP/3 force field, and molecular dynamic with the simulated annealing (SA) algorithm. The structures obtained by the first method show a better fit between the NMR spectral evidence and the calculation for all the peptides.
Acta Biochim Pol 2004
PMID:Solution structure of conformationally restricted vasopressin analogues. 1509 23

The vasopressin V2 receptor (V2R) belongs to the Class A G protein-coupled receptors (GPCRs). V2R is expressed in the renal collecting duct (CD), where it mediates the antidiuretic action of the neurohypophyseal hormone arginine vasopressin (CYFQNCPRG-NH2, AVP). Desmopressin ([1-deamino, 8-D]AVP, dDAVP) is strong selective V2R agonist with negligible pressor and uterotonic activity. In this paper, the interactions responsible for binding of dDAVP to vasopressin V2 receptor versus vasopressin V1a and oxytocin receptors has been examined. Three-dimensional activated models of the receptors were constructed using the multiple sequence alignment and the complex of activated rhodopsin with Gt(alpha) C-terminal peptide of transducin MII-Gt(alpha) (338-350) prototype (Slusarz, R.; Ciarkowski, J. Acta Biochim Pol 2004 51, 129-136) as a template. The 1-ns unconstrained molecular dynamics (MD) of receptor-dDAVP complexes immersed in the fully hydrated 1-palmitoyl-2-oleoyl-sn-glycero-3-phosphatidylcholine (POPC) membrane model was conducted in an Amber 7.0 force field. Highly conserved transmembrane residues have been proposed as being responsible for V2R activation and G protein coupling. Molecular mechanism of the dDAVP binding has been suggested. The internal water molecules involved in an intricate network of the hydrogen bonds inside the receptor cavity have been identified and their role in the stabilization of the agonist-bound state proposed.
 ...
PMID:Investigation of mechanism of desmopressin binding in vasopressin V2 receptor versus vasopressin V1a and oxytocin receptors: molecular dynamics simulation of the agonist-bound state in the membrane-aqueous system. 1633 59

In some cases diabetes insipidus may be induced by taking medications. In this article we report the case of a 58-year-old man with manifest polyuria induced by colchicine administered because of a gout attack. Interestingly, similar symptoms were observed 6 years earlier after treatment with gentamycin. In the described state of the examined patient early detection of the disease, colchicine withdrawal and temporary amiloride (and indometacin) administration led to a full normalisation of the patient's clinical status. A similar reaction to two different drugs responsible for only a small percentage of iatrogenic diabetes insipidus suggests that some patients may exhibit a general "hypersensitivity" to the development of a drug-induced vasopressin resistance and that patients with the history of iatrogenic diabetes insipidus should not be treated or should be treated cautiously with other drugs known to induce vasopressin-resistant polyuria.
Pol Arch Med Wewn 2005 Sep
PMID:[Nephrogenic diabetes insipidus induced by colchicine--a case report]. 1670 63

Treatment with some drugs may lead to the syndrome of inappropriate antidiuretic hormone secretion (SIADH), the presence of which is more likely in some populations, including people who are elderly or who take diuretics. Resulting drug-induced hyponatremia is often mild and usually resolves following water restriction and withdrawal of the drug. In some patients, however, it may be a potentially fatal condition that is typically asymptomatic until it becomes severe. In this article, we describe the case of a 59-year-old man with arterial hypertension, already treated with hydrochlorothiazide, who presented with hyponatremia after starting administration of carbamazepine. After excluding other common causes of hyponatremia, a diagnosis of SIADH was established, carbamazepine was withdrawn and SIADH treatment introduced. Our study shows that routine assessment of blood electrolytes is reasonable not only in patients receiving diuretics but also in patients treated with other drugs affecting vasopressin secretion.
Pol Arch Med Wewn 2007 Apr
PMID:[Carbamazepine-induced hyponatremia]. 1772 79

Hyponatremia is the most frequently encountered electrolyte disturbance in hospitalized patients. It is usually caused by dysregulation of arginine vasopressin (AVP) homeostasis which accompanies disorders associated with water retention such as congestive heart failure and cirrhosis, or follows euvolemic states such as syndrome of inapprioprate secretion of antidiuretic hormone. Available therapy, i.e. restriction of fluid intake, saline and diuretics, is often ineffective with unpredictable results and potentially serious side effects. Recent clinical trials with non-peptide AVP receptor antagonists (vaptans) have indicated that these drugs are effective in the treatment of hyponatremia. Vaptans lead to aquaresis, an electrolyte-sparing excretion of free water, that results in the correction of serum sodium concentration. Until now the Food and Drug Administration in the USA has approved the use of intravenous conivaptan for treatment of euvolemic hyponatremia. In this article, we review results from recent clinical trials on vaptans (lixivaptan, tolvaptan, conivaptan and satavaptan) which showed their efficacy in the treatment of hyponatremia.
Pol Arch Med Wewn 2007 Aug
PMID:[Vasopressin antagonists in treatment of hyponatremia]. 1801 83


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