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IP3-activated Ca2+ channels in the plasma membrane of cultured vascular endothelial cells
Ist Teil von
American Journal of Physiology: Cell Physiology, 1995-09, Vol.269 (3), p.C733-C738
Ort / Verlag
United States
Erscheinungsjahr
1995
Link zum Volltext
Quelle
MEDLINE
Beschreibungen/Notizen
L. Vaca and D. L. Kunze
Department of Molecular Physiology and Biophysics, Baylor College of Medicine, Houston, Texas 77030, USA.
Although it is clear that D-myo-inositol 1,4,5-trisphosphate (IP3) plays an
important role in the activation of Ca2+ influx, the mechanisms by which
this occurs remain controversial. In an attempt to determine the role of
IP3 in the activation of Ca2+ influx, patch-clamp single-channel
experiments in the cell-attached, inside-out, and outside-out
configurations were performed on cultured bovine aortic endothelial cells
(BAEC). The results presented indicate that both IP3 and intracellular Ca2+
can modulate the activity of a Ca(2+)-selective channel found in the plasma
membrane of these cells. Addition of 10 microM IP3 increased channel open
probability (P(o)) from a control value of 0.12 +/- 0.05 to 0.7 +/- 0.13 at
a constant intracellular Ca2+ of 1 nM in excised inside-out patches.
D-Myo-inositol 1,3,4,5-tetrakisphosphate at 50 microM was ineffective in
altering channel P(o). Channel activity declined after approximately 2 min
in the continuous presence of IP3. Three to four minutes after addition of
IP3, channel P(o) was reduced from 0.7 +/- 0.2 to 0.2 +/- 0.1, indicating
that an additional regulator might be required to maintain channel activity
in excised patches. The channel was reversibly blocked by application of 1
microgram/ml heparin to the intracellular side of inside-out patches. This
Ca(2+)-selective channel is indistinguishable from the depletion-activated
Ca2+ channel we have previously described in BAEC.