Control of H(+)-HCO3- plasma membrane transporters by urea hyperosmolality in rat medullary thick ascending limb
Details
Serval ID
serval:BIB_767855372B4C
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Control of H(+)-HCO3- plasma membrane transporters by urea hyperosmolality in rat medullary thick ascending limb
Journal
Am J Physiol
ISSN-L
0002-9513 (Print) 0002-9513 (Linking)
Publication state
Published
Issued date
1994
Volume
266
Number
5 Pt 1
Pages
C1157-64
Notes
Leviel, F
Froissart, M
Soualmia, H
Poggioli, J
Paillard, M
Bichara, M
eng
Research Support, Non-U.S. Gov't
1994/05/01
Am J Physiol. 1994 May;266(5 Pt 1):C1157-64.
Froissart, M
Soualmia, H
Poggioli, J
Paillard, M
Bichara, M
eng
Research Support, Non-U.S. Gov't
1994/05/01
Am J Physiol. 1994 May;266(5 Pt 1):C1157-64.
Abstract
Hyperosmolality inhibits bicarbonate absorption by the rat medullary thick ascending limb (MTAL) by unknown mechanisms. Intracellular pH (pHi) was monitored with use of 2',7'-bis(carboxyethyl)-5(6)-carboxyfluorescein in rat MTAL tubule suspensions to specify the H(+)-HCO3- membrane transporters affected by hyperosmolality. Measurements were made after > or = 15-min incubation of the cells in media rendered hypertonic by urea to avoid any change in cell volume. Na(+)-H+ antiport activity, estimated from the Na(+)-induced initial rate of pHi recovery of Na(+)-depleted acidified cells in the presence of 0.1 mM furosemide to inhibit Na(+)-K(+)-2Cl- cotransport, was inhibited by 300 mM urea and 10(-8) M arginine vasopressin (AVP) in an additive manner. Na(+)-H+ antiport inhibition by urea hyperosmolality was maximal at 300 mM urea with a half-maximal inhibitory concentration of 75 mM and was due to a 28% decrease in maximum velocity (Vmax) with no effect on the Michaelis constant for sodium. Urea hyperosmolality (300 mM) did not affect steady-state intracellular calcium concentration ([Ca2+]i), assessed with use of fura 2 fluorescence, and still inhibited Na(+)-H+ antiport in MTAL cells loaded with 1,2-bis(2- aminophenoxy)ethane-N,N,N',N'-tetraacetic acid to minimize any transient change in [Ca2+]i during the preincubation in urea medium. Furthermore, 300 mM urea did not stimulate basal or AVP-induced adenosine 3',5'-cyclic monophosphate (cAMP) accumulation. Plasma membrane H(+)-adenosinetriphosphatase (ATPase) activity and HCO3- transport, assessed by appropriate experimental protocols, were unaltered by 300 mM urea.(ABSTRACT TRUNCATED AT 250 WORDS)
Keywords
1-Methyl-3-isobutylxanthine/pharmacology, Animals, Antiporters/*metabolism, Bicarbonates/metabolism, Cell Membrane/drug effects/metabolism, Cyclic AMP/metabolism, *Hydrogen-Ion Concentration, Hypertonic Solutions, Kidney Medulla/*metabolism, Kinetics, Male, Proton-Translocating ATPases/metabolism, Rats, Rats, Sprague-Dawley, Sodium-Hydrogen Antiporter/antagonists & inhibitors, Time Factors, Urea/*pharmacology
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