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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1A
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pubmed:dateCreated |
1989-6-19
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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.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Calcium Channel Blockers,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium Channels,
http://linkedlifedata.com/resource/pubmed/chemical/Gallopamil,
http://linkedlifedata.com/resource/pubmed/chemical/Nitrendipine,
http://linkedlifedata.com/resource/pubmed/chemical/Potassium Channels
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pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
0004-4172
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
39
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
120-6
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:2541731-Animals,
pubmed-meshheading:2541731-Calcium Channel Blockers,
pubmed-meshheading:2541731-Calcium Channels,
pubmed-meshheading:2541731-Cells, Cultured,
pubmed-meshheading:2541731-Gallopamil,
pubmed-meshheading:2541731-Muscle, Smooth, Vascular,
pubmed-meshheading:2541731-Muscle Contraction,
pubmed-meshheading:2541731-Nitrendipine,
pubmed-meshheading:2541731-Potassium Channels,
pubmed-meshheading:2541731-Swine
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pubmed:year |
1989
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pubmed:articleTitle |
Pharmacological modulation of calcium and potassium channels in isolated vascular smooth muscle cells.
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pubmed:affiliation |
Lehrstuhl für angewandte Physiologie der Universität zu Köln, Fed. Rep. of Germany.
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pubmed:publicationType |
Journal Article,
In Vitro
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