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)

Massive hemorrhage from diverticular disease of the colon is a very difficult problem in abdominal emergency surgery. The pathogenesis of bleeding colonic diverticulosis is strictly correlated to the angioarchitecture of the colonic diverticular wall. Here the vasa recta penetrate the colonic wall from the serosa to the submucosa through connective tissue septa. Injurious factors arising from the colonic or diverticular lumen can produce an eccentric damage to the luminal side with intimal thickening, segmental weakening of the artery and its rupture with massive bleeding. Conventional barium enema is not able to show the source of the hemorrhage in the majority of the bleeding patients; colonoscopy, as primary emergency procedure, has significant positive findings in 41.5%-83.7% of patients. Radionuclide bleeding scans have a sensitivity rate of 86%-94%. Emergency arteriography localizes the bleeding source in higher rates ranging from 58% to 86% and is successful after intraarterial infusion of vasopressin or embolization in 47%-92% of patients. Surgical treatment for continued bleeding from diverticular disease is controversy. Segmental resection should be performed on patients with localized bleeding sources (positive arteriogram). Laparotomy, anterograde irrigation and intraoperative colonoscopy are indicated in patients with multiple bleeding sites and negative arteriography. Because the right colon is the most common site of bleeding in same cases is necessary to perform a subtotal colectomy with ileorectal anastomosis. Blind resections particularly in the elderly patients present high rebleeding rate (> 60%) and high mortality (30%) with sepsis accounting for the majority of deaths.
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PMID:[Massive hemorrhage caused by colonic diverticulosis]. 797 52

Arginine vasopressin (AVP) receptors are expressed early in the developing spinal cord. To characterize AVP-induced conductances in lower thoracic sympathetic preganglionic (SPN) and other lateral horn neurons, we used patch-clamp recording techniques in neonatal (11-21 days) rat spinal cord slices. Most (90%) of 273 neurons, including all 68 SPNs, responded to AVP with membrane depolarization and/or a V1 receptor-mediated, dose-dependent (0.01-1.0 microM) and tetrodotoxin (TTX)-resistant inward current. A role for G-proteins was indicated by persistence of this inward current after intracellular dialysis with GTP-gamma-S or GMP-PNP, its marked reduction with GDP-beta-S, and significant reduction, but not abolition, after preincubation with pertussis toxin or in the presence of N-ethylmaleimide. Analysis of individual current-voltage (I-V) relationships in 57 cells indicated the presence of two different membrane conductances. In 21 cells, net AVP-induced currents reversed around -103 mV, reflecting reduction in one or more barium-sensitive potassium conductances; in 12 cells, net AVP-induced current reversed around -40 mV and was not significantly sensitive to several potassium channel blockers including barium, tetraethylammonium chloride (TEA), 4-aminopyridine (4AP), cesium, or glibenclamide, suggesting increase in a nonselective cationic conductance that was separate from Ih; in 24 cells where I-V lines shifted in parallel, AVP-induced inward currents were significantly greater and probably involved both conductances. These data indicate that SPNs and a majority of unidentified neonatal lateral horn neurons possess functional G-protein-coupled V1-type vasopressin receptors. The wide distribution of AVP receptors in neonatal spinal lateral column cells suggests a role that may extend beyond involvement in regulation of autonomic nervous system function.
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PMID:Vasopressin-induced currents in rat neonatal spinal lateral horn neurons are G-protein mediated and involve two conductances. 977 48

Causes of pediatric gastrointestinal (GI) bleeding in children are numerous. The role of radiology in defining associated pathology, pinpointing the bleeding site, and intervening to control hemorrhage is discussed here. Barium studies, computed tomography (CT), and magnetic resonance imaging (MRI) each may play a role in identifying the underlying pathology associated with the bleeding. The exact source of bleeding may be localized by means of nuclear scintigraphy as well as selective angiography. In cases of life-threatening or persistent hemorrhage, once a bleeding source is identified, the interventional radiologist may offer percutaneous transcatheter therapy with selective intraarterial vasopressin infusion or embolotherapy.
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PMID:Imaging and radiological interventional techniques for gastrointestinal bleeding in children. 1057 28

Absorption of NH(4)(+) by the medullary thick ascending limb (MTAL) is a key event in the renal handling of NH(4)(+), leading to accumulation of NH(4)(+)/NH(3) in the renal medulla, which favors NH(4)(+) secretion in medullary collecting ducts and excretion in urine. The Na(+)-K(+)(NH(4)(+))-2Cl(-) cotransporter (BSC1/NKCC2) ensures approximately 50-65% of MTAL active luminal NH(4)(+) uptake under basal conditions. Apical barium- and verapamil-sensitive K(+)/NH(4)(+) antiport and amiloride-sensitive NH(4)(+) conductance account for the rest of active luminal NH(4)(+) transport. The presence of a K(+)/NH(4)(+) antiport besides BSC1 allows NH(4)(+) and NaCl absorption by MTAL to be independently regulated by vasopressin. At the basolateral step, the roles of NH(3) diffusion coupled to Na(+)/H(+) exchange or Na(+)/NH(4)(+) exchange, which favors NH(4)(+) absorption, and of Na(+)/K(+)(NH(4)(+))-ATPase, NH(4)(+)-Cl(-) cotransport, and NH(4)(+) conductance, which oppose NH(4)(+) absorption, have not been quantitatively defined. The increased ability of the MTAL to absorb NH(4)(+) during chronic metabolic acidosis involves an increase in BSC1 expression, but fine regulation of MTAL NH(4)(+) transport probably requires coordinated effects on various apical and basolateral MTAL carriers.
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PMID:Ammonium carriers in medullary thick ascending limb. 1113 9

The GABAB receptors GABAB-R1 and GABAB-R2 have been cloned in several mammalian species, and the functional receptor has been shown to exist as a heterodimeric complex. We have cloned guinea pig GABAB-R1 and GABAB-R2 receptor sequences and, using in situ hybridization and immunocytochemistry for vasopressin (AVP), we found that GABAB-R1 and -R2 receptors are expressed in vasopressin neurones of the supraoptic (SON) and paraventricular nuclei (PVN). Therefore, we used both sharp electrode and whole-cell patch recording techniques to examine the effects of the selective GABAB agonist baclofen on SON and PVN magnocellular neurones and to determine the coupling of the GABAB receptor to effector pathways. Recordings were made in coronal hypothalamic slices from both female (ovariectomized) and male guinea pigs. In the presence of tetrodotoxin (TTX), baclofen hyperpolarized (DeltaVmax = 5.6 mV, EC50 = 2.3 microM) SON magnocellular neurones (n = 27) under current clamp, or induced an outward current that reversed at EK (DeltaImax = 24.2 pA) in PVN magnocellular neurones (n = 33) under voltage clamp. Seventeen of the 24 biocytin-labelled SON magnocellular neurones were identified as AVP neurones, and ten of the 33 biocytin-labelled PVN neurones were identified as AVP or neurophysin-containing neurones, although all of the cells were clustered in the vasopressin-rich core. In the absence of TTX, baclofen activated an outward K+ current that hyperpolarized SON and PVN neurones and significantly reduced their firing rate. The outward current showed inward rectification and was blocked by the K+ channel blocker barium and the GABAB receptor antagonist CGP 35348. Therefore, GABAB receptors are coupled to inwardly rectifying K+ channels in SON and PVN magnocellular neurones and may play a prominent role in modulating phasic bursting activity in guinea pig vasopressin neurones.
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PMID:Baclofen inhibits guinea pig magnocellular neurones via activation of an inwardly rectifying K+ conductance. 1281 53

L-type Ca2+ channel activity was measured in L6 cells as nifedipine-sensitive barium (Ba2+; 5 mM) influx in a depolarizing salt solution containing 140 mM KCl. Addition of AVP (arginine-vasopressin) during Ba2+ uptake reduced the rate of Ba2+ influx by 60-100%; this was followed by a gradual restoration of the initial rate of Ba2+ uptake. Blockade of PKC (protein kinase C) by pretreatment with 10 muM bisindolylmaleimide did not affect the initial inhibition of Ba2+ influx, but completely abolished the recovery phase. The effect of AVP was half-maximal at 10 nM AVP and was blocked by the V1a receptor antagonist d-(CH2)(5)-Tyr(Me)-AVP. Activation of G(alphas) by isoprenaline or cholera toxin antagonized the actions of AVP on Ba2+ uptake. This protection persisted in the presence of the PKA (protein kinase A) inhibitor KT5720, and was not mimicked by agents that increase cAMP. Inhibition of Ba2+ influx was also elicited by ATP and ET (endothelin 1) with an order of effectiveness ET<ATP<AVP. Each of these agents has been reported to act through G(q)-coupled receptors. We conclude that activation of G(q)-coupled receptors produces a rapid inhibition of the cardiac L-type Ca2+ channel, which is subsequently overcome by activation of PKC.
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PMID:Regulation of the cardiac L-type calcium channel in L6 cells by arginine-vasopressin. 1691 57

Arginine-vasopressin (AVP) promotes muscle differentiation, hypertrophy, and regeneration through the combined activation of the calcineurin and Calcium/Calmodulin-dependent Protein Kinase (CaMK) pathways. The AVP system is impaired in several neuromuscular diseases, suggesting that AVP may act as a physiological factor in skeletal muscle. Since the Phosphoinositide 3-kinases/Protein Kinase B/mammalian Target Of Rapamycin (PI3K/Akt/mTOR) signaling plays a significant role in regulating muscle mass, we evaluated its role in the AVP myogenic effect. In L6 cells AKT1 expression was knocked down, and the AVP-dependent expression of mTOR and Forkhead box O3 (FoxO) was analyzed by Western blotting. The effect of the PI3K inhibitor LY294002 was evaluated by cellular and molecular techniques. Akt knockdown hampered the AVP-dependent mTOR expression while increased the levels of FoxO transcription factor. LY294002 treatment inhibited the AVP-dependent expression of Myocyte Enhancer Factor-2 (MEF2) and myogenin and prevented the nuclear translocation of MEF2. LY294002 also repressed the AVP-dependent nuclear export of histone deacetylase 4 (HDAC4) interfering with the formation of multifactorial complexes on the myogenin promoter. We demonstrate that the PI3K/Akt pathway is essential for the full myogenic effect of AVP and that, by targeting this pathway, one may highlight novel strategies to counteract muscle wasting in aging or neuromuscular disorders.
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PMID:Inhibition of Phosphoinositide 3-Kinase/Protein Kinase B Signaling Hampers the Vasopressin-dependent Stimulation of Myogenic Differentiation. 3146 43


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