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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
6
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pubmed:dateCreated |
1992-3-24
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pubmed:abstractText |
We have investigated hypertension-associated alterations in intracellular cations in the kidney by measuring intracellular pH, free Mg2+, free Ca2+, and Na+ concentrations in perfused normotensive and hypertensive rat (8-14 weeks old) kidneys using 31P, 19F, and double quantum-filtered (DQ) 23Na NMR. The effects of both anoxia and ischemia on the 23Na DQ signal confirmed its ability to detect changes in intracellular Na+. However, there was a sizable contribution of the extracellular Na+ to the 23Na DQ signal of the kidney. The intracellular free Ca2+ concentration, measured using 19F NMR and 5,5'difluoro-1,2-bis(2-aminophenoxy)ethane N,N,N',N'-tetraacetic acid, also increased dramatically during ischemia; the increase could be partly reversed by reperfusion. No significant differences were found between normotensive and hypertensive kidneys in the ATP level, intracellular pH, intracellular free Mg2+, and the 23Na DQ signal or in the extent of the extracellular contribution to the 23Na DQ signal. Oxygen consumption rates were also similar for the normotensive (5.02 +/- 0.46 mumol of O2/min/g) and hypertensive (5.47 +/- 0.42 mumol O2/min/g) rat kidneys. The absence of a significant difference in intracellular pH, Na+ concentration, and oxygen consumption between normotensive and hypertensive rat kidneys suggests that an alteration in the luminal Na+/H+ antiport activity in hypertension is unlikely. However, a highly significant increase (64%, p less than 0.01) in free Ca2+ concentration was found in perfused kidneys from hypertensive rats (557 +/- 48 nM, blood pressure = 199 +/- 5 mmHg, n = 6) compared with normotensive rats (339 +/- 21 nM, blood pressure = 134 +/- 6, n = 4) indicating altered renal calcium homeostasis in essential hypertension. An increase in intracellular free Ca2+ concentration without an accompanying change in the intracellular Na+ suggests, among many possibilities, that the Ca2+/Mg(2+)-ATPase may be inhibited in the hypertensive renal tissue.
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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/5,5'-difluoro-1,2-bis(2-aminophenoxy...,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium,
http://linkedlifedata.com/resource/pubmed/chemical/Cations,
http://linkedlifedata.com/resource/pubmed/chemical/Chelating Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Egtazic Acid,
http://linkedlifedata.com/resource/pubmed/chemical/Magnesium,
http://linkedlifedata.com/resource/pubmed/chemical/Sodium
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
0021-9258
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
25
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pubmed:volume |
267
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
3637-43
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:1740416-Animals,
pubmed-meshheading:1740416-Calcium,
pubmed-meshheading:1740416-Cations,
pubmed-meshheading:1740416-Chelating Agents,
pubmed-meshheading:1740416-Egtazic Acid,
pubmed-meshheading:1740416-Hydrogen-Ion Concentration,
pubmed-meshheading:1740416-Hypertension,
pubmed-meshheading:1740416-Ischemia,
pubmed-meshheading:1740416-Kidney,
pubmed-meshheading:1740416-Magnesium,
pubmed-meshheading:1740416-Magnetic Resonance Spectroscopy,
pubmed-meshheading:1740416-Perfusion,
pubmed-meshheading:1740416-Rats,
pubmed-meshheading:1740416-Rats, Inbred SHR,
pubmed-meshheading:1740416-Rats, Inbred WKY,
pubmed-meshheading:1740416-Sodium
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pubmed:year |
1992
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pubmed:articleTitle |
Multinuclear NMR studies of intracellular cations in perfused hypertensive rat kidney.
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pubmed:affiliation |
Department of Physiology and Biophysics, Albert Einstein College of Medicine, Bronx, New York 10461.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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