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Schuhmann, K; Groschner, K.
Protein kinase-C mediates dual modulation of L-type Ca2+ channels in human vascular smooth muscle.
FEBS Lett. 1994; 341(2-3):208-212 Doi: 10.1016/0014-5793(94)80458-3
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Leading authors Med Uni Graz
Groschner Klaus
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Abstract:
The role of protein kinase C (PKC) in cellular regulation of L-type Ca2+ channels was investigated in human umbilical vein smooth muscle. Activation of PKC, by low concentrations (< 30 nM) of 12-O-tetradecanoyl-phorbol-13-acetate (TPA) caused inhibition of Ca2+ channels, while higher concentrations of TPA (> 100 nM) elicited a transient rise, followed by sustained inhibition of Ca2+ channel activity in cell-attached patches. Low TPA concentrations predominantly reduced channel availability, while high concentrations of TPA (100 nM) transiently increased channel availability and, in addition, prolonged mean open time. The inactive 4-alpha-phorbol-12,13- didecanoate failed to affect channel activity, and pretreatment of the cells with PKC inhibitors (H-7, chelerythrine) antagonized inhibitory and stimulatory effects of TPA. Our results provide evidence for two distinct PKC-dependent mechanisms of L-type Ca2+ channel regulation in smooth muscle.
Find related publications in this database (using NLM MeSH Indexing)
Calcium Channels - drug effects Calcium Channels - metabolism
Humans -
Muscle, Smooth, Vascular - drug effects Muscle, Smooth, Vascular - enzymology Muscle, Smooth, Vascular - metabolism
Protein Kinase C - metabolism
Tetradecanoylphorbol Acetate - pharmacology

Find related publications in this database (Keywords)
L-TYPE CALCIUM CHANNEL
CELLULAR REGULATION
PHORBOL ESTER
PROTEIN KINASE-C
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