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)

Symptoms of hyponatremia and diuresis due to cerebral salt wasting syndrome (CSWS) are often observed after aneurysmal subarachnoid hemorrhage (SAH). Inadequately treated CSWS is known to work as a trigger of symptomatic vasospasm in SAH patients. Therefore, it is indispensable to detect and treat CSWS as early as possible in ICU. A 36-year-old man with SAH was admitted to our ICU. His urine volume increased excessively 3 days after ICU admission, and it reached a peak (39,250 ml x day(-1)) on the 6th day in ICU. Since infusion volume was controlled with regard to daily urinary output, hyponatremia was not noticeable and excessive urine volume stood out conspicuously. Though vasopressin and desmopressin were administered, the symptoms of natriuresis and hyponatremia were aggravated, associated with hyper secretion of natriuretic peptides (ANP 160 pg x dl(-1), BNP 172 pg x dl(-1)). Recent studies revealed that hyponatremia and hypovolemia following SAH might be caused by exaggerated secretion of natriuretic peptides. Experimental studies showed that the administration of vasopressin and desmopressin cause excessive secretion of natriuretic peptides under the circumstance of volume expansion in rats. We infer that the administration of vasopressin and desmopressin to our patient deterionated natriuresis in CSWS as in the previous experimental findings.
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PMID:[Case of cerebral salt wasting syndrome with difficulty in controling excessive urine volume]. 1736 22

We have investigated electron capture dissociation (ECD) of doubly protonated peptides with few or no basic amino acid residues (BAARs). For peptides containing one His, abundant b-type ions were only found when His was located adjacent to the N-terminus. Interestingly, b-type ions, particularly b(5)(+), were found to be the dominant product ions in ECD of peptides without BAARs. Fragmentation patterns of luteinizing hormone releasing hormone (LHRH) and vasopressin (VP), containing one Arg and one His, respectively, were compared to those of Q(8)-LHRH and oxytocin (OT) in which the BAAR is replaced with a non-BAAR. More b-type ions were found for Q(8)-LHRH and OT than for LHRH and VP. We also performed ECD of melittin and found no b-type ions from ECD of the 4+ charge state; however, many low abundance b-type ions were produced in ECD of the 5+ charge state. Possible mechanisms for the formation of b-type ions are discussed and we propose that such ions are formed as a consequence of protons being located at backbone amide nitrogens.
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PMID:Abundant b-type ions produced in electron capture dissociation of peptides without basic amino acid residues. 1790 79

The aim of the present study was to investigate the influence of melatonin on vasopressin (AVP) release from the rat hypothalamo-neurohypophysial (H-NH) system, both in vivo and in vitro, possibly modified by the peptide NK-1 and/or NK-2 receptor agonists and antagonists. Highly selective NK-1 receptor agonist, i.e., [Sar(9),Met(O(2))(11)]-Substance P, has been shown to enhance the AVP release from isolated rat H-NH system in vitro, while the NK-1 receptor antagonist--(Tyr(6),DPhe(7),D-His(9))-Substance P (6-11) as well as the NK-2 receptor selective agonist--(beta-Ala(8))-Neurokinin A (4-10) and antagonist--(Tyr(5),D-Trp(6,8,9),Lys-NH(2)(10))-Neurokinin A (4-10) were essentially inactive in modifying AVP secretion. Melatonin inhibited basal release of AVP but was not able to reduce significantly the in vitro response of vasopressinergic neurones to NK-1 receptor agonist. After intracerebroventricular (icv) administration, substance P (SP), neurokinin A (NKA) and the NK-1 receptor agonist (all at the concentration of 10(-7) M/L) significantly enhanced plasma AVP concentration. Such stimulatory effect of the latter peptide on AVP output from the eurohypophysis was reduced by an intravenous (iv) injection of melatonin, which itself (at a concentration of 5 ng/ml) caused a significant decrease in AVP release 10 min after injection. The inhibitory influence of melatonin on the AVP secretion was absent in rats injected icv with both tachykinin receptors antagonists, the NK-2 receptor agonist or NKA. The present data indicate a distinct role for NK-1 receptor in NKA/SP-mediated regulation of AVP release from the rat H-NH system. They have also shown that, under present experimental conditions, the stimulatory effect of NK-1 receptor activation on AVP secretion into the blood is sensitive to inhibitory influence of melatonin.
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PMID:Effect of melatonin on the vasopressin secretion as influenced by tachykinin NK-1 receptor agonist and antagonist: in vivo and in vitro studies. 1819 91

We report an 82-year old man prescribed paroxetine who had hyponatremia and in whom the syndrome of inappropriate secretion of antidiuretic hormone was diagnosed. He had taken sulpiride for depressed mental status. However, he showed parkinsonism, which was an adverse effect from the treatment of sulpiride. Therefore sulpiride was changed to selective serotonin reuptake inhibitor, paroxetine 10mg daily. His depressed mental status deteriorated after paroxetine treatment started. His depression had not lessened after 12 days, and the dosage was increased to 20mg daily. On the 15th day after starting paroxetine, routine laboratory tests showed that his serum sodium level was 126 mEq/l. We recognized that his confusion and loss of appetite were symptoms of hyponatremia, rather than of worsening depression. Laboratory data revealed hyponatremia, low serum osmolarity (242 mOsm/kg) with a relatively high level of serum antidiuretic hormone, and concentrated urine (439 mOsm/kg). We diagnosed the syndrome of inappropriate secretion of antidiuretic hormone (SIADH), associated with paroxetine. The dosage of paroxetine was reduced gradually and the serum sodium level returned to normal on day 2 after medication ceased completely. Paroxetine produces fewer adverse effects than other types of antidepressants. However, its use can be associated with inappropriate secretion of antidiuretic hormone in the body and may lead to SIADH, which is characterized by hyponatremia, a potentially fatal condition that is typically asymptomatic until it becomes severe. SIADH is more likely in some populations, including the elderly. Serum sodium levels should be monitored closely, especially in elderly patients.
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PMID:[Paroxetine-induced hyponatremia in an elderly man due to the syndrome of inappropriate secretion of antidiuretic hormone]. 1833 78

Vasoplegia resulting from severe burns may persist despite adequate fluid resuscitation and treatment with norepinephrine (NE), vasopressin (VP), and steroids. The adenylate cyclase inhibitor methylene blue (MB), currently used in the burn patient to treat methemoglobinemia, has been used to treat vasoplegia after cardiopulmonary bypass. We report the case of MB infusion in two burn patients refractory to NE. The patients had severe burns, 95 and 80% TBSA not responding to conventional treatment. Fluid requirements were estimated according to Parkland formula and then to maintain a urinary output of 30-50 ml/hr. Patient #1, 95% TBSA, was adrenally insufficient and was receiving steroids according to the Annane protocol, as well as VP at 0.2 U/min. His NE requirements were 55 mcg/kg/min. Patient #2, 80% TBSA, was receiving 20 mcg/kg/min of NE. Circulatory failure was defined as inability to maintain mean arterial pressure >70 mm Hg. Hemodynamic and physiologic parameters were measured before and after infusion of a single dose of 2 mg/kg of MB. Both patients showed dramatic improvements in their shock after MB. Patient #1 had an initial reaction within 30 minutes and reached peak effect at 1 hour. His NE requirements decreased to 0.2 mcg/kg/min and VP decreased to 0.04 U/min. Patient #2 showed effects within 15 minutes of the infusion and by 2 hours the NE was stopped. No adverse side effects were noted in either of the two patients. The fact that MB successfully reversed refractory vasoplegia after severe burns suggests a new tool for treating a small subgroup of patients who exhibit persistent vasoplegia from their burn injury. A controlled randomized trial is needed to test its effects on a large number of patients and graft survival.
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PMID:Methylene blue in the treatment of vasoplegia following severe burns. 1835 4

It is well-known that glucagon increases fractional excretion of urea in rats after a protein intravenous infusion. This effect was investigated by using: (a) in vitro microperfusion technique to measure [(14)C]-urea permeability (Pu x 10(-5)cm/s) in inner medullary collecting ducts (IMCD) from normal rats in the presence of 10(-7)M of glucagon and in the absence of vasopressin and (b) immunoblot techniques to determine urea transporter expression in tubule suspension incubated with the same glucagon concentration. Seven groups of IMCDs (n = 47) were studied. Our results revealed that: (a) glucagon decreased urea reabsorption dose-dependently; (b) the glucagon antagonist des-His(1)-[Glu(9)], blocked the glucagon action but not vasopressin action; (c) the phorbol myristate acetate, decreased urea reabsorption but (d) staurosporin, restored its effect; e) staurosporin decreased glucagon action, and finally, (f) glucagon decreased UT-A1 expression. We can conclude that glucagon reduces UT-A1 expression via a glucagon receptor by stimulating PKC.
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PMID:PKC stimulated by glucagon decreases UT-A1 urea transporter expression in rat IMCD. 1844 63

A new vasopressin analogue, [His1,6]AVP, was synthesized and characterized by potentiometric measurements as well as by UV-Vis, CD and EPR spectroscopy. At the physiological pH the peptide forms a stable complex with Cu2+ ions which is characterized by the {NH2, NIm, NIm(macrochelate)} binding mode. The replacement of both Cys by His residues in the vasopressin sequence results in a very significant increase in the efficiency of Cu2+ binding.
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PMID:The unusual binding abilities of the His-analogue of Arg-vasopressin towards Cu2+. 1880 8

A recalcitrant rheumatoid arthritis patient taking low dose weekly methotrexate was given oral 2-chlorodeoxyadenosine (cladribine) for 8 months in a multicenter trial. He developed dual infections over the course of the trial: disseminated herpes zoster and staphylococcal arthritis of the right elbow. His disseminated herpes zoster started with severe, unremitting abdominal pain caused by a gastric ulcer, followed by disseminated cutaneous herpes, hepatitis, pancreatitis, encephalitis, homonymous hemianopsia, the syndrome of inappropriate secretion of antidiuretic hormone (ADH), and malabsorption. Both the herpes zoster and S. aureus infections required prolonged proper chemotherapies. Serious, complicated viral, bacterial, or other unusual infections should be considered in patients with severe rheumatoid conditions treated with combination immunosuppressive therapy.
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PMID:Disseminated herpes zoster and s. Aureus septic arthritis in a rheumatoid arthritis patient treated with 2-chlorodeoxyadenosine (cladribine) and methotrexate. 1907 80

Nephrogenic syndrome of inappropriate antidiuresis is a recently identified genetic disease first described in two unrelated male infants with severe symptomatic hyponatremia. Despite undetectable arginine vasopressin levels, patients have inappropriately concentrated urine resulting in hyponatremia, hypoosmolality, and natriuresis. It was found that each infant had a different mutation of the vasopressin type II receptor (V2R) at codon 137 where arginine was converted to cysteine or leucine (R137C or R137L), resulting in constitutive signaling. Interestingly, a missense mutation at the same codon, converting arginine to histidine (R137H), leads to the opposite disease phenotype with a loss of the kidney's ability to concentrate urine resulting in nephrogenic diabetes insipidus. This mutation is associated with impaired signaling, although whether this is predominantly due to impaired trafficking to the plasma membrane, agonist-independent internalization, or G protein uncoupling is currently unclear. Using bioluminescence resonance energy transfer and confocal microscopy, we demonstrate that both V2R-R137C and V2R-R137L mutants interact with beta-arrestins in an agonist-independent manner resulting in dynamin-dependent internalization. This phenotype is similar to that observed for V2R-R137H, which is intriguing considering that it is accompanied by constitutive rather than impaired signaling. Consequently, it would seem that agonist-independent internalization per se is unlikely to be the major determinant of impaired V2R-R137H signaling. Our findings indicate that the V2R-R137C and V2R-R137L mutants traffic considerably more efficiently to the plasma membrane than V2R-R137H, identifying this as a potentially important mutation-dependent difference affecting V2R function.
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PMID:Agonist-independent interactions between beta-arrestins and mutant vasopressin type II receptors associated with nephrogenic syndrome of inappropriate antidiuresis. 1917 80

We have characterized the interaction between the Zn(2+) ions and the histidine analogues of oxytocin and arginine-vasopressin. Potentiometric methods were used for the determination of the stoichiometry of the complexes formed and the calculation of their stability constants. The NMR measurements revealed detailed structures of the complexes and confirmed the binding mode at physiological pH.
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PMID:Histidine analogues of oxytocin and vasopressin as efficient ligands for Zn2+ ions--potentiometric and NMR studies. 1951 25


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