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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
20
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pubmed:dateCreated |
1996-11-25
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pubmed:abstractText |
In endothelial cells, stretch-activated cation channels have been proposed to act as mechanosensors for changes in hemodynamic forces. We have identified a novel mechanosensitive pressure-activated channel in intact endothelium from rat aorta and mesenteric artery. The 18-pS cation channel responded with a multifold increase in channel activity when positive pressure was applied to the luminal cell surface with the patch pipette and inactivated at negative pipette pressure. Channel permeability ratio for K+, Na+, and Ca2+ ions was 1:0.98:0.23. Ca2+ influx through the channel was sufficient to activate a neighboring Ca2(+)-dependent K+ channel. Hemodynamic forces are chronically disturbed in arterial hypertension. Endothelial cell dysfunction has been implicated in the pathogenesis of arterial hypertension. In two comparative studies, density of the pressure-activated channel was found to be significantly higher in spontaneously hypertensive rats and renovascular hypertensive rats compared with their respective normotensive controls. Channel activity presumably leads to mechanosensitive Ca2+ influx and induces cell hyperpolarization by K+ channel activity. Both Ca2+ influx and hyperpolarization are known to induce a vasodilatory endothelial response by stimulating endothelial nitric oxide (NO) production. Up-regulation of channel density in hypertension could, therefore, represent a counterregulatory mechanism of vascular endothelium.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/8855342-1282158,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8855342-1690807,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8855342-1691450,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8855342-1700363,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8855342-1727681,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8855342-1856157,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8855342-2110114,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8855342-2355955,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8855342-2380245,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8855342-2381766,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8855342-2434860,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8855342-2444709,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8855342-2448637,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8855342-2536958,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8855342-2545495,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8855342-2573351,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8855342-3080370,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8855342-3260580,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8855342-6086918,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8855342-6270629,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8855342-6442314,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8855342-7510889,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8855342-7528629,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8855342-7531175,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8855342-7537813,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8855342-7539405,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8855342-7624393,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8855342-7679792,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8855342-7930552,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8855342-7963502,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8855342-7987028,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8855342-8118950,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8855342-8127330,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8855342-8406663
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
0027-8424
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
93
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
11253-8
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:8855342-Animals,
pubmed-meshheading:8855342-Calcium,
pubmed-meshheading:8855342-Calcium Channels,
pubmed-meshheading:8855342-Endothelium, Vascular,
pubmed-meshheading:8855342-Hemodynamics,
pubmed-meshheading:8855342-Hydrostatic Pressure,
pubmed-meshheading:8855342-Hypertension,
pubmed-meshheading:8855342-Hypertension, Renal,
pubmed-meshheading:8855342-Mechanoreceptors,
pubmed-meshheading:8855342-Rats,
pubmed-meshheading:8855342-Rats, Inbred SHR,
pubmed-meshheading:8855342-Rats, Inbred WKY,
pubmed-meshheading:8855342-Up-Regulation
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pubmed:year |
1996
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pubmed:articleTitle |
Up-regulation of pressure-activated Ca(2+)-permeable cation channel in intact vascular endothelium of hypertensive rats.
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pubmed:affiliation |
Division of Nephrology, University Hospital Benjamin Franklin, Free University of Berlin, Germany.
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pubmed:publicationType |
Journal Article,
In Vitro,
Research Support, Non-U.S. Gov't
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