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| rdf:type | |
| lifeskim:mentions | |
| pubmed:dateCreated |
1992-5-7
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| pubmed:abstractText |
1. Whole-cell patch clamp was combined with microspectrofluometry (Indo-1) to study the effects of bath applied ATP on membrane currents and cytoplasmic Ca2+ concentration ([Ca2+]i) in single smooth muscle cells of the guinea-pig urinary bladder. Experiments were carried out at 22 degrees C and in 3.6 mM [Ca2+]o. Superimposed K+ currents were reduced by Cs+ dialysis from the patch electrode. 2. At -60 mV, ATP induced an inward current (Ins,ATP) that peaked within 0.4 s and then decayed. Ins,ATP was activated half-maximally by 1.1 microM-ATP and saturated at 50 microM-ATP to -1.1 +/- 0.2 nA (mean +/- S.E.M.). At 3.6 mM [Ca2+]o, Ins,ATP had a reversal potential (Erev) of -5 +/- 2 mV. From the shifts in Erev during changes in [Na+]o or [Ca2+]o we estimated that approximately 7% of Ins,ATP is carried by Ca2+ ions. 3. ATP (50 microM) increased [Ca2+]i transiently from resting 130 +/- 40 nM to 730 +/- 100 nM. At 22 degrees C, [Ca2+]i rose at a rate proportional to the instantaneous current amplitude of Ins,ATP. This relation was lost, however, after warming to 36 degrees C which increased the peak Ins,ATP (Q10 = 1.25) but reduced the peak of the ATP induced [Ca2+]i transient (Q10 = 0.75). We suggest that warming to 36 degrees C stimulated Ca2+ sequestration and Ca2+ efflux to such a degree that peak [Ca2+]i was attenuated significantly. 4. The contribution of Ca2+ ions to Ins,ATP was evaluated from a comparison of the increments in [Ca2+]i due to Ins,ATP and due to L-type Ca2+ channel current (ICa). For the same increment, Ins,ATP had to transport 19 times more charge than ICa. This number suggests that 5.8 +/- 0.8% of Ins,ATP is carried by Ca2+ ions which can be translated into a permeability ratio of PNa:PCa approximately 1:1. 5. During bath application of ATP, peak ICa was inhibited by 80 +/- 15%. Inhibition of ICa diminished to 20 +/- 8% after cell dialysis with 40 mM-EGTA, and it was 19 +/- 7% when extracellular Ca2+ had been substituted by Ba2+. These results are in agreement with the hypothesis of 'ICa inactivation by Ca2+'. Depletion of intracellular Ca2+ stores by pre-treatment with 20 mM-caffeine did not attenuate significantly the ATP-induced rise in [Ca2+]i or the ATP-induced inhibition of ICa. 6. The ATP-induced [Ca2+]i transients and the reduction of peak ICa recovered along a similar time course.(ABSTRACT TRUNCATED AT 400 WORDS)
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| pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/1666653-1663160,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1666653-1696154,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1666653-1697199,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1666653-1697946,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1666653-1701681,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1666653-2155470,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1666653-2158070,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1666653-2391657,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1666653-2417191,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1666653-2417192,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1666653-2428640,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1666653-2439921,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1666653-2448060,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1666653-2559977,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1666653-2764093,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1666653-2908125,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1666653-3116214,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1666653-3838314,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1666653-3840439,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1666653-6095365,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1666653-6135390,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1666653-6297936,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1666653-6431088,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1666653-6498270,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1666653-7195747
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical | |
| pubmed:status |
MEDLINE
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| pubmed:issn |
0022-3751
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:volume |
440
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
479-96
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| pubmed:dateRevised |
2009-11-18
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| pubmed:meshHeading |
pubmed-meshheading:1666653-Adenosine Triphosphate,
pubmed-meshheading:1666653-Animals,
pubmed-meshheading:1666653-Calcium,
pubmed-meshheading:1666653-Calcium Channels,
pubmed-meshheading:1666653-Cells, Cultured,
pubmed-meshheading:1666653-Electrophysiology,
pubmed-meshheading:1666653-Guinea Pigs,
pubmed-meshheading:1666653-Ion Channel Gating,
pubmed-meshheading:1666653-Muscle, Smooth,
pubmed-meshheading:1666653-Urinary Bladder
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| pubmed:year |
1991
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| pubmed:articleTitle |
Ca2+ influx through ATP-gated channels increments [Ca2+]i and inactivates ICa in myocytes from guinea-pig urinary bladder.
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| pubmed:affiliation |
Department of Physiology, University of Cologne, Germany.
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| pubmed:publicationType |
Journal Article
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