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  • 11
    In: Bone, Elsevier BV, Vol. 29, No. 4 ( 2001-10), p. 393-402
    Type of Medium: Online Resource
    ISSN: 8756-3282
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2001
    detail.hit.zdb_id: 1496324-3
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  • 12
    Online Resource
    Online Resource
    American Physiological Society ; 1986
    In:  American Journal of Physiology-Gastrointestinal and Liver Physiology Vol. 251, No. 3 ( 1986-09-01), p. G382-G390
    In: American Journal of Physiology-Gastrointestinal and Liver Physiology, American Physiological Society, Vol. 251, No. 3 ( 1986-09-01), p. G382-G390
    Abstract: Apical membrane vesicles were prepared from proximal and distal segments of the large intestine of the rat by a method based on morphological criteria and were used to determine 22Na uptake. In both preparations an outwardly directed proton gradient stimulated 22Na uptake. In proximal colon a decrease in vesicular volume induced by an increased media osmolarity led to diminished 22Na uptake at 90 min; a significant (50-60%) portion of uptake represented binding. Initial uptake was linear for 10 s and extrapolated through zero, indicating minimal extravesicular binding. Initial uptake was a saturable function of medium Na concentration. In both preparations initial influx of 0.1 mM NaCl was inhibited by amiloride (0.1-1.0 mM), 15 mM NaCl, 15 mM LiCl, and 15 mM NH4Cl. From the characteristics of the initial 22Na influx we conclude that the apical membrane from colonocytes of proximal and distal segments contains a Na-H exchange with properties similar to those described in other epithelia.
    Type of Medium: Online Resource
    ISSN: 0193-1857 , 1522-1547
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1986
    detail.hit.zdb_id: 1477329-6
    SSG: 12
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  • 13
    Online Resource
    Online Resource
    Springer Science and Business Media LLC ; 1978
    In:  Pfl�gers Archiv European Journal of Physiology Vol. 373, No. 3 ( 1978-3), p. 243-248
    In: Pfl�gers Archiv European Journal of Physiology, Springer Science and Business Media LLC, Vol. 373, No. 3 ( 1978-3), p. 243-248
    Type of Medium: Online Resource
    ISSN: 0031-6768 , 1432-2013
    RVK:
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 1978
    detail.hit.zdb_id: 1463014-X
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  • 14
    Online Resource
    Online Resource
    Springer Science and Business Media LLC ; 1988
    In:  La Ricerca in Clinica e in Laboratorio Vol. 18, No. 4 ( 1988-10), p. 330-373
    In: La Ricerca in Clinica e in Laboratorio, Springer Science and Business Media LLC, Vol. 18, No. 4 ( 1988-10), p. 330-373
    Type of Medium: Online Resource
    ISSN: 0390-5748
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 1988
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  • 15
    Online Resource
    Online Resource
    Portland Press Ltd. ; 1977
    In:  Biochemical Journal Vol. 168, No. 3 ( 1977-12-15), p. 529-532
    In: Biochemical Journal, Portland Press Ltd., Vol. 168, No. 3 ( 1977-12-15), p. 529-532
    Abstract: Uptake of L-alanine and L-phenylalanine by purified bursh-border-membrane vesicles isolated from human small intestine was investigated by using a rapid-filtration technique. L-Alanine entered the same osmotically reactive space as D-glucose, indicating that transport into the vesicle rather than binding to the membranes was being observed. The uptake rate for L-alanine was higher in the presence of a Na+ gradient than in the presence of a K+ gradient. In the presence of a Na+ gradient, the lipophilic anion SCN- caused an increase in L-alanine transport, whereas the nearly impermeant SO42- anion decreased the uptake of L-alanine compared with its uptake in the presence of Cl-. The uptake of L-phenylalanine into the brush-border-membrane vesicle was also stimulated by Na+. The results indicate co-transport of Na+ and neutral amino acids inthe human intestinal brush-border membrane.
    Type of Medium: Online Resource
    ISSN: 0264-6021
    RVK:
    Language: English
    Publisher: Portland Press Ltd.
    Publication Date: 1977
    detail.hit.zdb_id: 1473095-9
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  • 16
    Online Resource
    Online Resource
    American Physiological Society ; 1990
    In:  American Journal of Physiology-Cell Physiology Vol. 259, No. 1 ( 1990-07-01), p. C121-C133
    In: American Journal of Physiology-Cell Physiology, American Physiological Society, Vol. 259, No. 1 ( 1990-07-01), p. C121-C133
    Abstract: Opossum kidney (OK) cells (an established cell line) were loaded with 2',7'-bis(2-carboxyethyl)-5,6-carboxyfluorescein (BCECF; a fluorescent dye with a pH-sensitive spectrum), and intracellular pH (pHi) was examined by microfluorometry. Single cells, within a confluent monolayer and grown on a permeant support, were examined for the mechanism of recovery from an acid load as imposed by exposure to ammonium chloride (NH4 prepulse). The Na(+)-dependent recovery of pHi from an acid load (Na(+)-H+ exchange) is examined in terms of the Na+ activation kinetics of the recovery and the polarity of the response. In 80% of the cells examined (33/41), both apical and basolateral Na+ cause recovery from an acid load. The response of cells to apical Na+ is well fit by Michaelis-Menten kinetics [Kt(Na) = 35 mM], but the response to basolateral Na+ is not. The response to basolateral Na+ addition is modeled in terms of variable transepithelial leak of Na+ and variable amounts of basolateral Na(+)-H+ exchange. Despite an average response to basolateral (145 mM) Na+ that is 34% of the response to apical Na+, modeling suggests that basolateral Na(+)-H+ exchange must be less than 10% of the cellular total to fit the basolateral Na+ activation kinetics. The model, and experiments using ordered addition of Na+ from the apical vs. basolateral medium, also suggest that transepithelial leak (of basolateral Na+ to the apical compartment) is required to explain the pHi recovery observed due to addition of basolateral Na+. Direct estimation of (basolateral to apical) transepithelial leak demonstrates that the response due to basolateral Na+ addition is explained by transepithelial leak and a Na(+)-H+ exchange that is expressed solely in the apical membrane.
    Type of Medium: Online Resource
    ISSN: 0363-6143 , 1522-1563
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1990
    detail.hit.zdb_id: 1477334-X
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  • 17
    Online Resource
    Online Resource
    American Physiological Society ; 1996
    In:  American Journal of Physiology-Renal Physiology Vol. 271, No. 4 ( 1996-10-01), p. F926-F930
    In: American Journal of Physiology-Renal Physiology, American Physiological Society, Vol. 271, No. 4 ( 1996-10-01), p. F926-F930
    Abstract: Heavy metal intoxication with Hg2+, Pb2+ and Cd2+ commonly leads to phosphaturia. In this study, we examined the effects of these heavy metals on Pi-induced currents (Ip) through NaPi-3, the human renal cotransporter for Na+ and Pi. Hg2+ inhibited Ip in a dose- and time-dependent fashion. Hg2+ decreased the extrapolated maximal current but did not alter the apparent affinity for Pi. This inhibition was also observed with the membrane-permeable oxidizing agent 2,2'-dithio-bis(5-nitropyridine) (DTNP) but not with the membrane-impermeable 5,5'-dithiobis(2-nitrobenzoic acid). Hg(2+)- and DTNP-mediated inhibition of Ip was reversible only in the presence of the reducing agent 2,3-dihydroxybutane-1,4-dithiol. Cd2+ and Pb2+ also inhibited Ip. However, while CD2+ did not significantly alter the apparent affinity for Pi, the apparent concentration needed for half-maximal current (Km) for Pi was increased by Pb2+. In contrast to Hg2+, the inhibition of Ip by Cd2+ and Pb2+ was rapidly reversible upon washout. In the presence of the Na(+)-K(+)-adenosinetriphosphatase inhibitor ouabain, Ip was not reduced, and the effects of the heavy metals were maintained. In summary, the three heavy metals Hg2+, Cd2+, and Pb2+ inhibit Ip through the Na+/Pi cotransporter NaPi-3 by distinct mechanisms. Heavy metal-mediated inhibition of NaPi-3 may be responsible for the phosphaturia observed after intoxication with these compounds.
    Type of Medium: Online Resource
    ISSN: 1931-857X , 1522-1466
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1996
    detail.hit.zdb_id: 1477287-5
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  • 18
    Online Resource
    Online Resource
    American Physiological Society ; 1986
    In:  American Journal of Physiology-Gastrointestinal and Liver Physiology Vol. 251, No. 2 ( 1986-08-01), p. G223-G229
    In: American Journal of Physiology-Gastrointestinal and Liver Physiology, American Physiological Society, Vol. 251, No. 2 ( 1986-08-01), p. G223-G229
    Abstract: The Ca2+ pump in rat duodenal epithelium is studied as ATP-dependent Ca2+ uptake in a vesicle preparation with a 9-fold purification in Na+-K+-ATPase activity and a 20-fold purification of Na+-K+-ATPase with respect to an endoplasmic reticulum marker. ATP-dependent Ca2+ uptake is reduced by 60% by digitonin treatment of the vesicles, whereas high-affinity Ca2+-ATPase is stimulated by the same treatment. Different methods to deplete membrane preparations of calmodulin have been used. In EDTA osmotically shocked vesicles, calmodulin stimulated ATP-dependent Ca2+ transport up to 100% in a Ca2+ concentration-dependent manner. The duodenal Ca2+ pump is inhibited by calmodulin antagonists only at low Ca2+ concentrations and in membranes not depleted from calmodulin. Vitamin D-dependent Ca2+-binding protein (Mr = 10,000) in concentrations up to 5 microM did not affect the rate of ATP-dependent Ca2+ transport, either in Ca2+-EGTA-buffered solutions or in EGTA-free solutions. In membrane preparations from vitamin D-deficient rats, the effects of calmodulin and of Ca2+-binding protein were identical to the vitamin D-repleted control preparations. This excludes a specific effect of Ca2+-binding protein and calmodulin in the vitamin D dependency of duodenal Ca2+-ATPase.
    Type of Medium: Online Resource
    ISSN: 0193-1857 , 1522-1547
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1986
    detail.hit.zdb_id: 1477329-6
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  • 19
    Online Resource
    Online Resource
    American Physiological Society ; 1988
    In:  American Journal of Physiology-Cell Physiology Vol. 255, No. 1 ( 1988-07-01), p. C76-C85
    In: American Journal of Physiology-Cell Physiology, American Physiological Society, Vol. 255, No. 1 ( 1988-07-01), p. C76-C85
    Abstract: Suspensions of OK cells (a continuous epithelioid cell line from opossum kidney) are examined by electronic cell sizing, measurements of intracellular pH, and measurements of cellular Na+ and K+. The response of the cells to hypertonic solutions is evaluated in most detail. When shrunken by exposure to hyperosmotic medium (430 mosmol/kg), the cells do not demonstrate a regulatory volume increase (RVI) independent of the solute that is used to increase osmolality [NaCl, N-methyl-D-glucamine-HCl (NMGCl), or sucrose] . In contrast, when cells are preexposed to 190 mosmol/kg medium and then shrunken by exposure to 310 mosmol/kg medium, a volume increase is observed after the addition of 120 mosmol/kg NaCl or NMGCl, but not sucrose. This RVI is sensitive to 1 mM furosemide and removal of Na+ or K+ from the medium, but it is not inhibited by 1 mM amiloride. In the presence of a propionate-induced cellular acidification, a Na+-H+ exchanger in the cells is shown to have a large capacity for net solute uptake and to be inhibited by 1 mM amiloride. Net solute uptake by the Na+-H+ exchanger is sensitive to addition of parathyroid hormone or 8-bromoadenosine 3',5'-cyclic monophosphate but is not stimulated in response to cell shrinkage.
    Type of Medium: Online Resource
    ISSN: 0363-6143 , 1522-1563
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1988
    detail.hit.zdb_id: 1477334-X
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  • 20
    Online Resource
    Online Resource
    American Physiological Society ; 1989
    In:  American Journal of Physiology-Cell Physiology Vol. 256, No. 2 ( 1989-02-01), p. C252-C259
    In: American Journal of Physiology-Cell Physiology, American Physiological Society, Vol. 256, No. 2 ( 1989-02-01), p. C252-C259
    Abstract: Volume regulatory responses of OK cells (a continuous epithelioid cell line from opossum kidney) are examined by electronic cell sizing and measurements of intracellular pH in cell suspensions. In response to a 40% reduction in osmolality, the cells swell and then subsequently shrink toward their starting volume. This regulatory volume decrease (RVD) is reduced by replacement of Cl- in the medium with acetate. Replacement of Cl- with NO3- accelerates the RVD. The RVD response is inhibited by 1 mM quinine or 100 microM 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS) in the medium. The inhibitory effect of 100 microM DIDS (but not 1 mM quinine) is altered by replacement of Cl- by NO3- in the medium. Hypotonic challenge does not induce a DIDS-sensitive net flux of acid-base equivalents. Addition of (9 microM) valinomycin also inhibits the RVD response. It is suggested that the RVD response of OK cells involves activation of separate K+ and Cl- channels.
    Type of Medium: Online Resource
    ISSN: 0363-6143 , 1522-1563
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1989
    detail.hit.zdb_id: 1477334-X
    SSG: 12
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