The Experts below are selected from a list of 93 Experts worldwide ranked by ideXlab platform
J L Garvin - One of the best experts on this subject based on the ideXlab platform.
-
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.
-
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
Masahito Yamada - One of the best experts on this subject based on the ideXlab platform.
-
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.
N H Garcia - One of the best experts on this subject based on the ideXlab platform.
-
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.
-
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
Peter Hoglund - One of the best experts on this subject based on the ideXlab platform.
-
pharmacokinetics and antidiuretic effect of a new vasopressin analogue f992 in overhydrated male volunteers
European Journal of Clinical Pharmacology, 1999Co-Authors: T Callreus, J Lundahl, Anja Broeders, Peter HoglundAbstract:Objective: The aim of the present study was to study the pharmacokinetics, the antidiuretic effects and the safety of [D-Phe2, Thi3, α-Me-Abu4, Hyp7, D-Arg8]-dC1-vasopressin, a new antidiuretic peptide (F992, Ferring, Sweden), administered as intravenous infusion to orally overhydrated male volunteers.
Hiroro Nakano - One of the best experts on this subject based on the ideXlab platform.
-
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.