Source:http://linkedlifedata.com/resource/pubmed/id/15292047
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
6
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pubmed:dateCreated |
2004-11-3
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pubmed:abstractText |
In the medullary thick ascending limb (MTAL) of rat kidney, inhibiting basolateral Na(+)/H(+) exchange with either amiloride or nerve growth factor (NGF) results secondarily in inhibition of apical Na(+)/H(+) exchange, thereby decreasing transepithelial HCO(3)(-) absorption. To assess the possible role of the Na(+)/H(+) exchanger NHE1 in this regulatory process, MTALs from wild-type and NHE1 knockout (NHE1(-/-)) mice were studied using in vitro microperfusion. The rate of HCO(3)(-) absorption was decreased 60% in NHE1(-/-) MTALs (15.4 +/- 0.5 pmol.min(-1).mm(-1) wild-type vs. 6.0 +/- 0.5 pmol.min(-1).mm(-1) NHE1(-/-)). Transepithelial voltage, an index of the NaCl absorption rate, did not differ in wild-type and NHE1(-/-) MTALs. Basolateral addition of 10 microM amiloride or 0.7 nM NGF decreased HCO(3)(-) absorption by 45-49% in wild-type MTALs but had no effect on HCO(3)(-) absorption in NHE1(-/-) MTALs. Inhibition of HCO(3)(-) absorption by vasopressin and stimulation by hyposmolality, both of which regulate MTAL HCO(3)(-) absorption through primary effects on apical Na(+)/H(+) exchange, were similar in wild-type and NHE1(-/-) MTALs. Thus the regulatory defect in NHE1(-/-) MTALs is specific for factors (bath amiloride and NGF) shown previously to inhibit HCO(3)(-) absorption through primary effects on basolateral Na(+)/H(+) exchange. These findings demonstrate a novel role for NHE1 in transepithelial HCO(3)(-) absorption in the MTAL, in which basolateral NHE1 controls the activity of apical NHE3. Paradoxically, a reduction in NHE1-mediated H(+) extrusion across the basolateral membrane leads to a decrease in apical Na(+)/H(+) exchange activity that reduces HCO(3)(-) absorption.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Amiloride,
http://linkedlifedata.com/resource/pubmed/chemical/Arginine Vasopressin,
http://linkedlifedata.com/resource/pubmed/chemical/Bicarbonates,
http://linkedlifedata.com/resource/pubmed/chemical/Cation Transport Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Membrane Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Nerve Growth Factor,
http://linkedlifedata.com/resource/pubmed/chemical/Slc9a1 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Sodium-Hydrogen Antiporter
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pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
1931-857X
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
287
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
F1244-9
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pubmed:dateRevised |
2011-4-28
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pubmed:meshHeading |
pubmed-meshheading:15292047-Absorption,
pubmed-meshheading:15292047-Amiloride,
pubmed-meshheading:15292047-Animals,
pubmed-meshheading:15292047-Arginine Vasopressin,
pubmed-meshheading:15292047-Bicarbonates,
pubmed-meshheading:15292047-Cation Transport Proteins,
pubmed-meshheading:15292047-Kidney Medulla,
pubmed-meshheading:15292047-Kinetics,
pubmed-meshheading:15292047-Loop of Henle,
pubmed-meshheading:15292047-Membrane Proteins,
pubmed-meshheading:15292047-Mice,
pubmed-meshheading:15292047-Mice, Knockout,
pubmed-meshheading:15292047-Nerve Growth Factor,
pubmed-meshheading:15292047-Osmolar Concentration,
pubmed-meshheading:15292047-Sodium-Hydrogen Antiporter
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pubmed:year |
2004
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pubmed:articleTitle |
Transepithelial HCO3- absorption is defective in renal thick ascending limbs from Na+/H+ exchanger NHE1 null mutant mice.
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pubmed:affiliation |
Department of Medicine, University of Texas Medical Branch, 301 Univ. Boulevard, Galveston, TX 77555, USA. dgood@utmb.edu
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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