Medizinische Universität Graz Austria/Österreich - Forschungsportal - Medical University of Graz
Gewählte Publikation:
Poteser, M; Wakabayashi, I; Rosker, C; Teubl, M; Schindl, R; Soldatov, NM; Romanin, C; Groschner, K.
Crosstalk between voltage-independent Ca2+ channels and L-type Ca2+ channels in A7r5 vascular smooth muscle cells at elevated intracellular pH: evidence for functional coupling between L-type Ca2+ channels and a 2-APB-sensitive cation channel.
Circ Res. 2003; 92(8):888-896
Doi: 10.1161/01.RES.0000069216.80612.66
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- Führende Autor*innen der Med Uni Graz
- Groschner Klaus
- Poteser Michael
- Co-Autor*innen der Med Uni Graz
- Rosker Christian
- Schindl Rainer
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- Abstract:
- This study was designed to investigate the role of voltage-independent and voltage-dependent Ca2+ channels in the Ca2+ signaling associated with intracellular alkalinization in A7r5 vascular smooth muscle cells. Extracellular administration of ammonium chloride (20 mmol/L) resulted in elevation of intracellular pH and activation of a sustained Ca2+ entry that was inhibited by 2-amino-ethoxydiphenyl borate (2-APB, 200 micromol/L) but not by verapamil (10 micro;mol/L). Alkalosis-induced Ca2+ entry was mediated by a voltage-independent cation conductance that allowed permeation of Ca2+ (PCa/PNa approximately 6), and was associated with inhibition of L-type Ca2+ currents. Alkalosis-induced inhibition of L-type Ca2+ currents was dependent on the presence of extracellular Ca2+ and was prevented by expression of a dominant-negative mutant of calmodulin. In the absence of extracellular Ca2+, with Ba2+ or Na+ as charge carrier, intracellular alkalosis failed to inhibit but potentiated L-type Ca2+ channel currents. Inhibition of Ca2+ currents through voltage-independent cation channels by 2-APB prevented alkalosis-induced inhibition of L-type Ca2+ currents. Similarly, 2-APB prevented vasopressin-induced activation of nonselective cation channels and inhibition of L-type Ca2+ currents. We suggest the existence of a pH-controlled Ca2+ entry pathway that governs the activity of smooth muscle L-type Ca2+ channels due to control of Ca2+/calmodulin-dependent negative feedback regulation. This Ca2+ entry pathway exhibits striking similarity with the pathway activated by stimulation of phospholipase-C-coupled receptors, and may involve a similar type of cation channel. We demonstrate for the first time the tight functional coupling between these voltage-independent Ca2+ channels and classical voltage-gated L-type Ca2+ channels.
- Find related publications in this database (using NLM MeSH Indexing)
- Ammonium Chloride - pharmacology
- Animals -
- Arginine Vasopressin - pharmacology
- Barium - pharmacology
- Boron Compounds - pharmacology
- Calcium - metabolism
- Calcium - pharmacology
- Calcium Channels - physiology
- Calcium Channels, L-Type - physiology
- Calmodulin - genetics
- Calmodulin - metabolism
- Cell Line -
- Humans -
- Hydrogen-Ion Concentration -
- Membrane Potentials - drug effects
- Muscle, Smooth, Vascular - cytology
- Muscle, Smooth, Vascular - drug effects
- Muscle, Smooth, Vascular - physiology
- Time Factors -
- Find related publications in this database (Keywords)
- intracellular pH
- Ca2+ channels
- nonselective cation channels
- 2-APB
- smooth muscle