| pubmed-article:2414440 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:2414440 | lifeskim:mentions | umls-concept:C0006675 | lld:lifeskim |
| pubmed-article:2414440 | lifeskim:mentions | umls-concept:C0034493 | lld:lifeskim |
| pubmed-article:2414440 | lifeskim:mentions | umls-concept:C0003483 | lld:lifeskim |
| pubmed-article:2414440 | lifeskim:mentions | umls-concept:C0028351 | lld:lifeskim |
| pubmed-article:2414440 | lifeskim:mentions | umls-concept:C0032821 | lld:lifeskim |
| pubmed-article:2414440 | lifeskim:mentions | umls-concept:C2348693 | lld:lifeskim |
| pubmed-article:2414440 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
| pubmed-article:2414440 | lifeskim:mentions | umls-concept:C0439536 | lld:lifeskim |
| pubmed-article:2414440 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:2414440 | pubmed:dateCreated | 1985-12-16 | lld:pubmed |
| pubmed-article:2414440 | 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. | lld:pubmed |
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| pubmed-article:2414440 | pubmed:language | eng | lld:pubmed |
| pubmed-article:2414440 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:2414440 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:2414440 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:2414440 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:2414440 | pubmed:issn | 0022-3751 | lld:pubmed |
| pubmed-article:2414440 | pubmed:author | pubmed-author:JonesA WAW | lld:pubmed |
| pubmed-article:2414440 | pubmed:author | pubmed-author:AaronsonP IPI | lld:pubmed |
| pubmed-article:2414440 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:2414440 | pubmed:volume | 367 | lld:pubmed |
| pubmed-article:2414440 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:2414440 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:2414440 | pubmed:pagination | 27-43 | lld:pubmed |
| pubmed-article:2414440 | pubmed:dateRevised | 2010-9-7 | lld:pubmed |
| pubmed-article:2414440 | pubmed:meshHeading | pubmed-meshheading:2414440-... | lld:pubmed |
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| pubmed-article:2414440 | pubmed:meshHeading | pubmed-meshheading:2414440-... | lld:pubmed |
| pubmed-article:2414440 | pubmed:year | 1985 | lld:pubmed |
| pubmed-article:2414440 | pubmed:articleTitle | Calcium regulation of potassium fluxes in rabbit aorta during activation by noradrenaline or high potassium medium. | lld:pubmed |
| pubmed-article:2414440 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:2414440 | pubmed:publicationType | In Vitro | lld:pubmed |
| pubmed-article:2414440 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:2414440 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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