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Dissecting out the complex Ca2+-mediated phenylephrine-induced contractions of mouse aortic segments
Paul Fransen1, Cor E Van Hove2, Arthur J A Leloup1
1Department of Pharmaceutical Sciences, University of Antwerp, Antwerp, Belgium.
Plos One
|March 25, 2015
Summary
Vascular smooth muscle cells (VSMC) use L-type Ca2+ channels (VGCC) and non-selective cation channels (NSCC) for contractions. Small changes in membrane potential significantly impact Ca2+ influx and arterial function, suggesting NSCC blockers may be relevant for hypertension.
Area of Science:
- Cardiovascular Physiology
- Vascular Biology
- Smooth Muscle Cell Function
Background:
- L-type Ca2+ channel (VGCC) mediated Ca2+ influx in vascular smooth muscle cells (VSMC) is crucial for arterial stiffening and blood pressure regulation.
- The precise relationship between VGCC influx, steady-state contractions from α1-adrenoreceptor stimulation, and modulation by resting membrane potential (Vm) in VSMC remains unclear.
Purpose of the Study:
- To investigate the role of Ca2+ influx pathways, specifically VGCC and non-selective cation channels (NSCC), in α1-adrenoreceptor-mediated tonic contractions of aortic segments.
- To determine how small variations in VSMC resting membrane potential modulate Ca2+ influx and contractile performance.
- To explore the interplay between intracellular Ca2+ release and Ca2+ influx in regulating VSMC contractility.
Main Methods:
- Isometric tension measurements and Ca2+ mobilization studies in aortic segments from C57Bl6 mice stimulated with phenylephrine (PE).
- Analysis of the relationship between Ca2+ influx via VGCC and NSCC and the resulting tonic contractions.
- Investigation of the effect of modulating intracellular Ca2+ release on the relative contribution of VGCC and NSCC.
Main Results:
- α1-adrenoreceptor stimulation induced both phasic (intracellular Ca2+ release) and tonic (Ca2+ influx) contractions.
- Tonic contractions were dependent on Ca2+ influx through both VGCC (within a specific voltage window) and NSCC.
- Small alterations in VSMC membrane potential significantly impacted VGCC-mediated Ca2+ influx and overall contractile force.
- Modulating intracellular Ca2+ release altered the balance between VGCC and NSCC contributions to contraction.
Conclusions:
- α1-adrenoreceptor-mediated VSMC contraction involves complex interactions between intracellular Ca2+ release and Ca2+ influx via both VGCC and NSCC.
- Modulation of VSMC membrane potential critically influences Ca2+ influx and arterial contractile performance.
- These findings highlight a potential, previously underappreciated role for NSCC and NSCC blockers in arterial stiffening and hypertension, alongside the established role of VGCC.
