| pubmed-article:2541731 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:2541731 | lifeskim:mentions | umls-concept:C0006675 | lld:lifeskim |
| pubmed-article:2541731 | lifeskim:mentions | umls-concept:C0026844 | lld:lifeskim |
| pubmed-article:2541731 | lifeskim:mentions | umls-concept:C1135918 | lld:lifeskim |
| pubmed-article:2541731 | lifeskim:mentions | umls-concept:C0032824 | lld:lifeskim |
| pubmed-article:2541731 | lifeskim:mentions | umls-concept:C0205409 | lld:lifeskim |
| pubmed-article:2541731 | lifeskim:mentions | umls-concept:C0205464 | lld:lifeskim |
| pubmed-article:2541731 | lifeskim:mentions | umls-concept:C1709059 | lld:lifeskim |
| pubmed-article:2541731 | pubmed:issue | 1A | lld:pubmed |
| pubmed-article:2541731 | pubmed:dateCreated | 1989-6-19 | lld:pubmed |
| pubmed-article:2541731 | pubmed:abstractText | Calcium antagonists relax vascular smooth muscle cells (VSM) by decreasing Ca-influx and intracellular Ca-load. In isolated VSM, Ca-influx was measured as Ca-current by the voltage clamp technique applied to a patch of membrane (single-channel current) or to the whole cell (whole-cell current ICa). Gallopamil exerted Ca-antagonism mostly by reducing channel availability, i.e. the probability that the Ca-channel opens upon depolarization. Whole-cell-Ca-currents revealed prominent frequency dependence, i.e. reduction of ICa increased with the number of depolarizations. In addition, the gallopamil effect was voltage-dependent such that depolarized myocytes were more sensitive than hyperpolarized cells. The dihydropyridine nitrendipine abbreviated the life time which the Ca-channel stood in the open state and it hindered the channel to re-open again. Reduction of availability was found only after a prolonged application. In whole cell ICa, nitrendipine accelerated the inactivation time course. The Ca-antagonistic effect was voltage-dependent but not frequency-dependent. Potassium agonists are supposed to activate K-channels thereby hyperpolarizing the membrane, hyperpolarization shuts off the Ca-channels and thereby reduces Ca-influx. The K-agonists cromakalim, (+) niguldipine and diazoxide activated the Ca-dependent maxi K-channel (inside-out patches studied at [Ca2+]c of 50 nmol/l or 500 nmol/l. They increased the open probability mainly by decreasing the long closures between the channel openings. The K-agonists can repolarize the cell once it excited and suppress further excitability. | lld:pubmed |
| pubmed-article:2541731 | pubmed:language | eng | lld:pubmed |
| pubmed-article:2541731 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:2541731 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:2541731 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:2541731 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:2541731 | pubmed:month | Jan | lld:pubmed |
| pubmed-article:2541731 | pubmed:issn | 0004-4172 | lld:pubmed |
| pubmed-article:2541731 | pubmed:author | pubmed-author:IsenbergGG | lld:pubmed |
| pubmed-article:2541731 | pubmed:author | pubmed-author:KlöcknerUU | lld:pubmed |
| pubmed-article:2541731 | pubmed:author | pubmed-author:TrieschmannUU | lld:pubmed |
| pubmed-article:2541731 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:2541731 | pubmed:volume | 39 | lld:pubmed |
| pubmed-article:2541731 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:2541731 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:2541731 | pubmed:pagination | 120-6 | lld:pubmed |
| pubmed-article:2541731 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
| pubmed-article:2541731 | pubmed:meshHeading | pubmed-meshheading:2541731-... | lld:pubmed |
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| pubmed-article:2541731 | pubmed:meshHeading | pubmed-meshheading:2541731-... | lld:pubmed |
| pubmed-article:2541731 | pubmed:meshHeading | pubmed-meshheading:2541731-... | lld:pubmed |
| pubmed-article:2541731 | pubmed:meshHeading | pubmed-meshheading:2541731-... | lld:pubmed |
| pubmed-article:2541731 | pubmed:year | 1989 | lld:pubmed |
| pubmed-article:2541731 | pubmed:articleTitle | Pharmacological modulation of calcium and potassium channels in isolated vascular smooth muscle cells. | lld:pubmed |
| pubmed-article:2541731 | pubmed:affiliation | Lehrstuhl für angewandte Physiologie der Universität zu Köln, Fed. Rep. of Germany. | lld:pubmed |
| pubmed-article:2541731 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:2541731 | pubmed:publicationType | In Vitro | lld:pubmed |
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