The Experts below are selected from a list of 96 Experts worldwide ranked by ideXlab platform
Scott A. Rivkees - One of the best experts on this subject based on the ideXlab platform.
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Differentiating appropriate Antidiuretic hormone secretion, inappropriate Antidiuretic hormone secretion and cerebral salt wasting: the common, uncommon, and misnamed.
Current opinion in pediatrics, 2008Co-Authors: Scott A. RivkeesAbstract:Purpose of reviewCauses of hyponatremia in children include the syndrome of appropriate Antidiuretic hormone secretion, the syndrome of inappropriate Antidiuretic hormone secretion and cerebral salt wasting. The purpose of this review is to distinguish these possibilities, focusing on cerebral salt
D A Schooley - One of the best experts on this subject based on the ideXlab platform.
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Antidiuretic effects of a factor in brain corpora cardiaca corpora allata extract on fluid reabsorption across the cryptonephric complex of manduca sexta
The Journal of Experimental Biology, 2000Co-Authors: S Liao, N Audsley, D A SchooleyAbstract:Extracts of the brain/corpora cardiaca/corpora allata (Br/CC/CA) complex of Manduca sexta larvae elicit an Antidiuretic effect, measured by an increase in fluid reabsorption across the cryptonephric complex of larval M. sexta. Separation of the extract by reversed-phase liquid chromatography gave two fractions with Antidiuretic effects. The more potent of these two factors was further characterized for its effects on the cryptonephric complex. Its Antidiuretic effect is not inhibited by bumetanide, a drug that inhibits M. sexta diuretic hormone (Mas-DH)-stimulated fluid reabsorption. These data indicate that the mechanism of the Antidiuretic effect of the factor is different from that of Mas-DH on the cryptonephric complex. The basal reabsorption of the cryptonephric complex is blocked when treated on the lumen side with bafilomycin A(1), an inhibitor of the H(+)-ATPase, or with amiloride, an inhibitor of the H(+)/K(+) antiporter. However, the Antidiuretic-factor-stimulated fluid reabsorption is not affected by either bafilomycin A(1) or amiloride. The increase in reabsorption triggered by the semi-purified factor can be inhibited by Cl(−) channel blockers or by removing Cl(−) from the lumen side of the cryptonephric complex. It appears that this factor activates a Cl(−) pump associated with the cryptonephric complex. Forskolin mimics the effect of this factor on fluid reabsorption, and the effect of forskolin is not inhibited by bumetanide. A selective and potent inhibitor of protein kinase A, H-89, also inhibits Antidiuretic-factor-stimulated fluid reabsorption. Addition of the factor to cryptonephric complexes maintained in vitro caused a significant increase in cyclic AMP levels extracted from these tissues compared with values for controls. These data suggest that the Antidiuretic effect of the factor in Br/CC/CA extract is mediated by cyclic AMP.
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Antidiuretic effects of a factor in brain/corpora cardiaca/corpora allata extract on fluid reabsorption across the cryptonephric complex of Manduca sexta.
The Journal of experimental biology, 2000Co-Authors: S Liao, N Audsley, D A SchooleyAbstract:Extracts of the brain/corpora cardiaca/corpora allata (Br/CC/CA) complex of Manduca sexta larvae elicit an Antidiuretic effect, measured by an increase in fluid reabsorption across the cryptonephric complex of larval M. sexta. Separation of the extract by reversed-phase liquid chromatography gave two fractions with Antidiuretic effects. The more potent of these two factors was further characterized for its effects on the cryptonephric complex. Its Antidiuretic effect is not inhibited by bumetanide, a drug that inhibits M. sexta diuretic hormone (Mas-DH)-stimulated fluid reabsorption. These data indicate that the mechanism of the Antidiuretic effect of the factor is different from that of Mas-DH on the cryptonephric complex. The basal reabsorption of the cryptonephric complex is blocked when treated on the lumen side with bafilomycin A(1), an inhibitor of the H(+)-ATPase, or with amiloride, an inhibitor of the H(+)/K(+) antiporter. However, the Antidiuretic-factor-stimulated fluid reabsorption is not affected by either bafilomycin A(1) or amiloride. The increase in reabsorption triggered by the semi-purified factor can be inhibited by Cl(-) channel blockers or by removing Cl(-) from the lumen side of the cryptonephric complex. It appears that this factor activates a Cl(-) pump associated with the cryptonephric complex. Forskolin mimics the effect of this factor on fluid reabsorption, and the effect of forskolin is not inhibited by bumetanide. A selective and potent inhibitor of protein kinase A, H-89, also inhibits Antidiuretic-factor-stimulated fluid reabsorption. Addition of the factor to cryptonephric complexes maintained in vitro caused a significant increase in cyclic AMP levels extracted from these tissues compared with values for controls. These data suggest that the Antidiuretic effect of the factor in Br/CC/CA extract is mediated by cyclic AMP.
J L Garvin - One of the best experts on this subject based on the ideXlab platform.
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Mechanism of the nitric oxide-induced blockade of collecting duct water permeability.
Hypertension (Dallas Tex. : 1979), 1996Co-Authors: N H Garcia, B A Stoos, O A Carretero, J L GarvinAbstract:Nitric oxide has a diuretic effect in vivo. We have shown that nitric oxide inhibits Antidiuretic hormone-stimulated osmotic water permeability in the collecting duct; however, the mechanism by which this occurs is unknown. We hypothesized that inhibition of Antidiuretic hormone-stimulated water permeability by nitric oxide in the collecting duct is the result of activation of cGMP-dependent protein kinase, which in turn decreases intracellular cAMP. To test this hypothesis, we microperfused cortical collecting ducts. Antidiuretic hormone-stimulated water permeability was 317 +/- 47 microm/s (P < .001). Addition of spermine NONOate, a nitric oxide donor, to the bath decreased water permeability to 74 +/- 38 microm/s (P < .002). In the presence of LY 83583, an inhibitor of soluble guanylate cyclase, spermine NONOate did not change water permeability. Addition of spermine NONOate increased cGMP production (P < .01). In the presence of the cGMP-dependent protein kinase inhibitor, spermine NONOate did not change water permeability. Since Antidiuretic hormone increases water permeability by increasing cAMP, we hypothesized that nitric oxide inhibits water permeability by decreasing cAMP. In tubules pretreated with Antidiuretic hormone, intracellular cAMP was 18.9 +/- 3.9 fmol/mm. In tubules treated with Antidiuretic hormone and spermine NONOate, cAMP was 9.3 +/- 1.7 fmol/mm (P < .03). We also examined the effect of spermine NONOate on dibutyryl-cAMP-stimulated water permeability. In the presence of dibutyryl-cAMP, water permeability was 388 +/- 30 microm/s. Addition of spermine NONOate had no significant effect on water permeability. Time controls and inhibitors by themselves did not change Antidiuretic hormone-stimulated water permeability. We concluded that nitric oxide decreases Antidiuretic hormone-stimulated water permeability by increasing cGMP via soluble guanylate cyclase, activating cGMP-dependent protein kinase and decreasing cAMP.
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Mechanism of the Nitric Oxide-Induced Blockade of Collecting Duct Water Permeability
Hypertension, 1996Co-Authors: N H Garcia, B A Stoos, O A Carretero, J L GarvinAbstract:Abstract Nitric oxide has a diuretic effect in vivo. We have shown that nitric oxide inhibits Antidiuretic hormone–stimulated osmotic water permeability in the collecting duct; however, the mechanism by which this occurs is unknown. We hypothesized that inhibition of Antidiuretic hormone–stimulated water permeability by nitric oxide in the collecting duct is the result of activation of cGMP-dependent protein kinase, which in turn decreases intracellular cAMP. To test this hypothesis, we microperfused cortical collecting ducts. Antidiuretic hormone–stimulated water permeability was 317±47 μm/s ( P
Bernard Lammek - One of the best experts on this subject based on the ideXlab platform.
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The effects of N-terminal part modification of arginine vasopressin analogues with 2-aminoindane-2-carboxylic acid: a highly potent V2 agonist.
Journal of Medicinal Chemistry, 2007Co-Authors: Wioleta Kowalczyk, Dariusz Sobolewski, Adam Prahl, Izabela Derdowska, Lenka Borovičková, Jirina Slaninova, Bernard LammekAbstract:In this study we present the synthesis and some pharmacological properties of nine new analogues of arginine vasopressin modified in the N-terminal part of the molecule with 2-aminoindane-2-carboxylic acid (Aic). The peptides were tested for their in vitro uterotonic and in vivo pressor and Antidiuretic activities. One of the new peptides, [Mpa 1 ,Aic 2 ,Val 4 ,D-Arg 8 ]VP, exhibited an Antidiuretic activity similar to that of [Mpa 1 ,D-Arg 8 ]VP, thus being one of the most potent Antidiuretic vasopressin analogues reported to date.
Masahito Yamada - One of the best experts on this subject based on the ideXlab platform.
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Syndrome of inappropriate secretion of Antidiuretic hormone (SIADH) associated with lateral medullary syndrome: case report and literature review
BMC neurology, 2016Co-Authors: Hiroro Nakano, Daisuke Yanase, Masahito YamadaAbstract:Only one case of syndrome of inappropriate secretion of Antidiuretic hormone with lateral medullary syndrome has been reported so far. We report a case of lateral medullary syndrome showing syndrome of inappropriate secretion of Antidiuretic hormone and analyze the pathomechanism underlying its clinical features. A 67-year-old man was admitted to our hospital for dizziness, dysarthria, and dysphagia. He was diagnosed with lateral medullary syndrome based on the neurological examination and brain magnetic resonance imaging. Horner syndrome was absent. Asymptomatic hyponatremia appeared 9 days after admission and the patient was diagnosed with syndrome of inappropriate secretion of Antidiuretic hormone. Fluid restriction and intravenous furosemide injection improved the hyponatremia. Lateral medullary syndrome could be associated with syndrome of inappropriate secretion of Antidiuretic hormone.