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Mark A. Knepper - One of the best experts on this subject based on the ideXlab platform.
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vasopressin increases Water Permeability of kidney collecting duct by inducing translocation of aquaporin cd Water channels to plasma membrane
Proceedings of the National Academy of Sciences of the United States of America, 1995Co-Authors: Soren Nielsen, Chung-lin Chou, David Marples, Erik Ilso Christensen, Bellamkonda K Kishore, Mark A. KnepperAbstract:Water excretion by the kidney is regulated by the peptide hormone vasopressin. Vasopressin increases the Water Permeability of the renal collecting duct cells, allowing more Water to be reabsorbed from collecting duct urine to blood. Despite long-standing interest in this process, the mechanism of the Water Permeability increase has remained undetermined. Recently, a molecular Water channel (AQP-CD) has been cloned whose expression appears to be limited to the collecting duct. Previously, we immunolocalized this Water channel to the apical plasma membrane (APM) and to intracellular vesicles (IVs) of collecting duct cells. Here, we test the hypothesis that vasopressin increases cellular Water Permeability by inducing exocytosis of AQP-CD-laden vesicles, transferring Water channels from IVs to APM. Rat collecting ducts were perfused in vitro to determine Water Permeability and subcellular distribution of AQP-CD in the same tubules. The collecting ducts were fixed for immunoelectron microscopy before, during, and after exposure to vasopressin. Vasopressin exposure induced increases in Water Permeability and the absolute labeling density of AQP-CD in the APM. In parallel, the APM:IV labeling ratio increased. Furthermore, in response to vasopressin withdrawal, AQP-CD labeling density in the APM and the APM:IV labeling ratio decreased in parallel to a measured decrease in osmotic Water Permeability. We conclude that vasopressin increases the Water Permeability of collecting duct cells by inducing a reversible translocation of AQP-CD Water channels from IVs to the APM.
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In vitro perfusion of chinchilla thin limb segments: segmentation and osmotic Water Permeability
American Journal of Physiology-Renal Physiology, 1992Co-Authors: Chung-lin Chou, Mark A. KnepperAbstract:The thin limb segments of the long loop of Henle are thought to play important roles in the urinary concentrating mechanism. In this study, we present new approaches to the identification, dissection, and in vitro perfusion of individual thin limb segments from all levels of the chinchilla renal medulla, including the deepest portions of the papilla. We have applied these techniques to the investigation of the osmotic Water Permeability along the chinchilla long loop of Henle. The results demonstrate that the osmotic Water Permeability of the thin descending limb is not uniformly high along its length, as previously thought, but that the distal 20% of the long-loop descending limb has a very low Water Permeability (approximately 50 microns/s). The transition to the low Water Permeability region of the thin descending limb is accompanied by a relatively abrupt change in morphology (increased cellularity and decreased diameter) that is readily perceptible in the perfused segments and even in the dissection dish. In contrast, the upper part of the chinchilla long-loop thin descending limb had an extremely high osmotic Water Permeability (greater than 2,000 microns/s) as observed in other species. Thin ascending limbs from deep in the inner medulla had Water permeabilities that were indistinguishable from zero, as previously found in thin ascending limbs from near the inner-outer medullary junction. The presence of a low-Water-Permeability portion of the long-loop thin descending limb in chinchilla may have important implications with regard to the inner medullary concentrating process. A relatively low osmotic Water Permeability (397 microns/s) was also found in the deep inner medullary portion of the thin descending limb from the rat.
M. S. Brudnaya - One of the best experts on this subject based on the ideXlab platform.
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Prostaglandin-dependent osmotic Water Permeability of the frog and trout urinary bladder.
Comparative biochemistry and physiology. Part A Molecular & integrative physiology, 1998Co-Authors: Yu. V. Natochin, E. I. Shakhmatova, Ya. Yu. Komissarchik, E. S. Snigirevskaya, N. P. Prutskova, M. S. BrudnayaAbstract:Washout of autacoids from serosal Ringer solution, using a repeated change of the solution of the frog and trout urinary bladder, was accompanied by a pronounced rise in the osmotic Water Permeability: the Water transport in the frog rose from 0.05±0.02 to 1.21±0.26 μl min−1·cm−2, in the trout, from 0.041±0.011 to 0.26±0.034 μl min−1·cm−2. Such an increase in the osmotic Water Permeability in the trout and frog urinary bladder occurred in the background of a decrease in the prostaglandin E2 concentration in the serosal Ringer solution. This Permeability increase was accompanied by the formation of aggregates of intramembranous particles in the apical plasma membrane of the trout and frog urinary bladder. A decrease in the osmotic Water Permeability was achieved by the addition to the serosal Ringer solution of 10−8 M prostaglandin. Experiments on the frog urinary bladder have shown that prostaglandins E1, I2 and F2α also decrease the osmotic Water Permeability. Vasotocin increased the osmotic Water Permeability in the frog urinary bladder but did not affect the osmotic Water Permeability of the trout urinary bladder. The data obtained indicates a role of the endogenous prostaglandin production in maintaining the low osmotic Water Permeability in the frog and trout urinary bladder. A suggestion is made that in the vertebrate evolution, colonisation of the fresh-Water was connected with the maintenance of the low osmotic Water Permeability via participation of prostaglandins, whereas the vasotocin hydroosmotic effect developed in the vertebrate evolution later and provided for the possibility of the Water absorption, osmotic homeostasis and animal migration from fresh-Water to the land.
Chung-lin Chou - One of the best experts on this subject based on the ideXlab platform.
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vasopressin increases Water Permeability of kidney collecting duct by inducing translocation of aquaporin cd Water channels to plasma membrane
Proceedings of the National Academy of Sciences of the United States of America, 1995Co-Authors: Soren Nielsen, Chung-lin Chou, David Marples, Erik Ilso Christensen, Bellamkonda K Kishore, Mark A. KnepperAbstract:Water excretion by the kidney is regulated by the peptide hormone vasopressin. Vasopressin increases the Water Permeability of the renal collecting duct cells, allowing more Water to be reabsorbed from collecting duct urine to blood. Despite long-standing interest in this process, the mechanism of the Water Permeability increase has remained undetermined. Recently, a molecular Water channel (AQP-CD) has been cloned whose expression appears to be limited to the collecting duct. Previously, we immunolocalized this Water channel to the apical plasma membrane (APM) and to intracellular vesicles (IVs) of collecting duct cells. Here, we test the hypothesis that vasopressin increases cellular Water Permeability by inducing exocytosis of AQP-CD-laden vesicles, transferring Water channels from IVs to APM. Rat collecting ducts were perfused in vitro to determine Water Permeability and subcellular distribution of AQP-CD in the same tubules. The collecting ducts were fixed for immunoelectron microscopy before, during, and after exposure to vasopressin. Vasopressin exposure induced increases in Water Permeability and the absolute labeling density of AQP-CD in the APM. In parallel, the APM:IV labeling ratio increased. Furthermore, in response to vasopressin withdrawal, AQP-CD labeling density in the APM and the APM:IV labeling ratio decreased in parallel to a measured decrease in osmotic Water Permeability. We conclude that vasopressin increases the Water Permeability of collecting duct cells by inducing a reversible translocation of AQP-CD Water channels from IVs to the APM.
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In vitro perfusion of chinchilla thin limb segments: segmentation and osmotic Water Permeability
American Journal of Physiology-Renal Physiology, 1992Co-Authors: Chung-lin Chou, Mark A. KnepperAbstract:The thin limb segments of the long loop of Henle are thought to play important roles in the urinary concentrating mechanism. In this study, we present new approaches to the identification, dissection, and in vitro perfusion of individual thin limb segments from all levels of the chinchilla renal medulla, including the deepest portions of the papilla. We have applied these techniques to the investigation of the osmotic Water Permeability along the chinchilla long loop of Henle. The results demonstrate that the osmotic Water Permeability of the thin descending limb is not uniformly high along its length, as previously thought, but that the distal 20% of the long-loop descending limb has a very low Water Permeability (approximately 50 microns/s). The transition to the low Water Permeability region of the thin descending limb is accompanied by a relatively abrupt change in morphology (increased cellularity and decreased diameter) that is readily perceptible in the perfused segments and even in the dissection dish. In contrast, the upper part of the chinchilla long-loop thin descending limb had an extremely high osmotic Water Permeability (greater than 2,000 microns/s) as observed in other species. Thin ascending limbs from deep in the inner medulla had Water permeabilities that were indistinguishable from zero, as previously found in thin ascending limbs from near the inner-outer medullary junction. The presence of a low-Water-Permeability portion of the long-loop thin descending limb in chinchilla may have important implications with regard to the inner medullary concentrating process. A relatively low osmotic Water Permeability (397 microns/s) was also found in the deep inner medullary portion of the thin descending limb from the rat.
Philip W. Wertz - One of the best experts on this subject based on the ideXlab platform.
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Lipid Content and Water Permeability of Skin and Oral Mucosa
The Journal of investigative dermatology, 1991Co-Authors: Christopher A. Squier, Patrick Cox, Philip W. WertzAbstract:It has been claimed that total lipid content may be the critical factor determining the Water Permeability of skin. The present study examined this relationship in various oral epithelia and epidermis. Epithelia was heat separated from specimens of porcine skin, gingiva, buccal mucosa, palate, and floor of mouth. Lipids were solvent extracted and separated by thin layer chromatography with appropriate standards. The plates were sprayed with sulfuric acid and charred, and the concentration of lipids was determined by densitometry as mg lipid/gm tissue dry weight. Permeability constants were determined for each tissue by using tritiated Water in perfusion chambers. When these values were com- pared over all regions, total lipid did not appear to be related to the Permeability of these tissues. However, in the keratinized regions (epidermis, gingiva, and palate) a lower Water Permeability was related to a greater content of total lipid, nonpolar lipid, ceramide, and glucosylceramide. In non-keratinized tissues, a lower Permeability corresponded to in- creased amounts of an unidentified glycosylceramide. The role of lipid in the Permeability barrier of these tissues was further demonstrated by extracting specimens of skin and oral mucosa with chloroform/methanol and then determining Kp values; in both tissue regions, there was a significant increase in Water Permeability. Thus, although lipid is a component of the Water Permeability barrier in both skin and oral mucosa, different lipid components subserve this function in keratinized and non-keratinized tissues.
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
