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Inability of Ehrlich ascites tumor cells to volume regulate following a hyperosmotic challenge.
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- Author(s): Levinson C;Levinson C
- Source:
The Journal of membrane biology [J Membr Biol] 1991 May; Vol. 121 (3), pp. 279-88.
- Publication Type:
Journal Article; Research Support, U.S. Gov't, P.H.S.
- Language:
English
- Additional Information
- Source:
Publisher: Springer Country of Publication: United States NLM ID: 0211301 Publication Model: Print Cited Medium: Print ISSN: 0022-2631 (Print) Linking ISSN: 00222631 NLM ISO Abbreviation: J Membr Biol Subsets: MEDLINE
- Publication Information:
Original Publication: New York, Springer.
- Subject Terms:
- Abstract:
Ehrlich cells shrink when the osmolality of the suspending medium is increased and behave, at least initially, as osmometers. Subsequent behavior depends on the nature of the hyperosmotic solute but in no case did the cells exhibit regulatory volume increase. With hyperosmotic NaCl an osmometric response was found and the resultant volume maintained relatively constant. Continuous shrinkage was observed, however, with sucrose-induced hyperosmolality. In both cases increasing osmolality from 300 to 500 mOSM initiated significant changes in cellular electrolyte content, as well as intracellular pH. This was brought about by activation of the Na+/H+ exchanger, the Na/K pump, the Na+ + K+ + 2Cl cotransporter and by loss of K+ via a Ba-sensitive pathway. The cotransporter in response to elevated [Cl-]i (approximately 100 mM) and/or the increase in the outwardly directed gradient of chemical potential for Na+, K+ and Cl-, mediated net loss of ions which accounted for cell shrinkage in the sucrose-containing medium. In hyperosmotic NaCl, however, the net Cl- flux was almost zero suggesting minimal net cotransport activity. We conclude that volume stability following cell shrinkage depends on the transmembrane gradient of chemical potential for [Na+ + K+ + Cl-], as well as the ratio of intra- to extracellular [Cl-]. Both factors appear to influence the activity of the cotransport pathway.
- References:
J Cell Physiol. 1976 Jun;88(2):181-92. (PMID: 1270521)
Annu Rev Physiol. 1985;47:545-60. (PMID: 2581505)
J Cell Physiol. 1977 Nov;93(2):293-302. (PMID: 591564)
J Cell Physiol. 1972 Feb;79(1):73-7. (PMID: 5009379)
J Membr Biol. 1987;100(2):183-91. (PMID: 2828630)
J Cell Physiol. 1984 Jul;120(1):41-8. (PMID: 6736136)
J Membr Biol. 1985;87(2):121-30. (PMID: 2416928)
Biochim Biophys Acta. 1984 Jul 25;774(2):159-68. (PMID: 6743652)
J Gen Physiol. 1960 Nov;44:365-79. (PMID: 13713240)
Am J Physiol. 1990 Apr;258(4 Pt 1):C749-53. (PMID: 2333955)
Eur J Biochem. 1988 Feb 1;171(3):425-33. (PMID: 3345741)
J Cell Physiol. 1982 Feb;110(2):149-54. (PMID: 7068772)
J Membr Biol. 1985;87(2):93-105. (PMID: 2416931)
J Membr Biol. 1984;78(3):211-22. (PMID: 6427469)
Biochim Biophys Acta. 1989 Jan 18;988(1):73-97. (PMID: 2535787)
J Gen Physiol. 1983 Nov;82(5):619-38. (PMID: 6644271)
J Gen Physiol. 1985 May;85(5):765-87. (PMID: 2987392)
Biochim Biophys Acta. 1990 Jan 15;1021(1):1-8. (PMID: 2294960)
J Membr Biol. 1984;79(1):7-18. (PMID: 6737466)
Ann N Y Acad Sci. 1985;456:166-82. (PMID: 2418724)
J Gen Physiol. 1982 Jul;80(1):125-47. (PMID: 7119727)
J Membr Biol. 1986;91(2):147-55. (PMID: 3018257)
Pflugers Arch. 1987 May;408(5):432-7. (PMID: 3601633)
J Membr Biol. 1983;76(3):269-80. (PMID: 6100866)
J Gen Physiol. 1977 Jul;70(1):99-121. (PMID: 894253)
J Membr Biol. 1987;100(1):83-96. (PMID: 3430568)
Biochim Biophys Acta. 1982 Jun 28;688(3):740-6. (PMID: 7115702)
Physiol Rev. 1989 Apr;69(2):315-82. (PMID: 2538851)
Nature. 1982 Sep 9;299(5879):161-3. (PMID: 7110335)
- Grant Information:
CA 32927 United States CA NCI NIH HHS
- Accession Number:
0 (Chlorides)
0 (Saline Solution, Hypertonic)
9NEZ333N27 (Sodium)
RWP5GA015D (Potassium)
- Publication Date:
Date Created: 19910501 Date Completed: 19910909 Latest Revision: 20190820
- Publication Date:
20240829
- Accession Number:
10.1007/BF01951561
- Accession Number:
1865492
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