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rdf:type |
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lifeskim:mentions |
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pubmed:dateCreated |
1985-12-16
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pubmed:abstractText |
The dependency of noradrenaline- and depolarization-mediated increases in K permeability on cellular Ca was investigated by measuring the effect of diltiazem and Ca-free medium on stimulated 42K efflux and contracture. The increase in the rate constant (k) for 42K efflux induced by cellular depolarization with 80 mM-K was inhibited by 70% in the presence of 10(-5) M-diltiazem. The noradrenaline (NA)-mediated increase in k was only slightly suppressed by diltiazem at 10(-5) M-NA, but was inhibited by diltiazem in a dose-dependent fashion for a submaximal concentration of NA 10(-7) M. Similar inhibitory effects were observed on contractile responses. Basal 42K efflux progressively increased in a 0 Ca physiological salt solution (PSS) containing 2 mM-EGTA. This process was suppressed in a concentration-dependent manner as [Mg] was increased. In experiments utilizing 0 Ca PSS, [Mg] was therefore raised to 15 mM to maintain stable basal effluxes. Ca removal for 30 min reduced the 80 mM-K-mediated increase in k by 64%. The NA-induced increase in k became more transient in 0 Ca PSS with a progressive diminution in the magnitude of this response as the duration of Ca depletion was increased. The diminution of the 42K efflux response in 0 Ca PSS was well fitted by a mono-exponential function (half-time, t1/2 = 46 min). The NA-induced contracture in 0 Ca solution decreased with a biphasic time course subsequent to Ca removal. Intracellular Ca release by NA, measured by means of a 45Ca efflux protocol, decreased as a mono-exponential function of time, with a t 1/2 of 21 min. We conclude that both alpha-receptor activation and membrane depolarization increase K permeability largely as a result of increased cellular free [Ca]. The effect of depolarization appears to depend mainly on influx of extracellular Ca. NA increases both influx and intracellular release of Ca which serve to open K channels. The apparent release of cellular Ca as measured by 45Ca efflux into Ca-free solution decreased more rapidly, however, than did the NA stimulation of 42K efflux and tension. These observations may result from the presence of a slowly depleted Ca store which cannot be detected directly by measuring NA-induced release of 45Ca.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/2414440-13449874,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2414440-13618284,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2414440-190404,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2414440-19431570,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2414440-19747,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2414440-2579748,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2414440-352237,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2414440-4199367,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2414440-4356609,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2414440-4367920,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2414440-4443918,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2414440-533865,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2414440-5500784,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2414440-6092628,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2414440-6261986,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2414440-6275064,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2414440-6278954,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2414440-6296366,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2414440-6297828,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2414440-6297831,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2414440-6303206,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2414440-6308244,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2414440-6325217,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2414440-6798548,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2414440-6801256,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2414440-6833408,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2414440-7108782,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/2414440-7411461,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2414440-745248,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2414440-850203,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2414440-856939,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2414440-894254,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2414440-966174
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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 |
0022-3751
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
367
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
27-43
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pubmed:dateRevised |
2010-9-7
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pubmed:meshHeading |
pubmed-meshheading:2414440-Animals,
pubmed-meshheading:2414440-Aorta, Thoracic,
pubmed-meshheading:2414440-Calcium,
pubmed-meshheading:2414440-Diltiazem,
pubmed-meshheading:2414440-Egtazic Acid,
pubmed-meshheading:2414440-Ion Channels,
pubmed-meshheading:2414440-Muscle, Smooth, Vascular,
pubmed-meshheading:2414440-Norepinephrine,
pubmed-meshheading:2414440-Potassium,
pubmed-meshheading:2414440-Rabbits,
pubmed-meshheading:2414440-Time Factors,
pubmed-meshheading:2414440-Vasoconstriction
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pubmed:year |
1985
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pubmed:articleTitle |
Calcium regulation of potassium fluxes in rabbit aorta during activation by noradrenaline or high potassium medium.
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pubmed:publicationType |
Journal Article,
In Vitro,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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