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Large conductance Ca2+-activated K+ channels modulate endothelial cell outward currents and nitric oxide release in the intact rat superior mesenteric artery

Endothelial cells (EC) control vascular smooth muscle cell (VSMC) tone by release of paracrine factors. VSMC may also influence the EC layer, and therefore, the present study hypothesized that the opening of large-conductance Ca2+ activated K+ (BKCa) channels may indirectly modulate EC hyperpolariza...

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Bibliographic Details
Main Authors: Climent, Belén (Author) , Schubert, Rudolf (Author)
Format: Article (Journal)
Language:English
Published: 2012
In: Biochemical and biophysical research communications
Year: 2011, Volume: 417, Issue: 3, Pages: 1007-1013
ISSN:1090-2104
DOI:10.1016/j.bbrc.2011.12.076
Online Access:Verlag, kostenfrei, Volltext: http://dx.doi.org/10.1016/j.bbrc.2011.12.076
Verlag, kostenfrei, Volltext: http://www.sciencedirect.com/science/article/pii/S0006291X11022856
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Author Notes:Belén Climent, Rudolf Schubert, Edgaras Stankevicius, Albino García-Sacristán, Ulf Simonsen, Luis Rivera
Description
Summary:Endothelial cells (EC) control vascular smooth muscle cell (VSMC) tone by release of paracrine factors. VSMC may also influence the EC layer, and therefore, the present study hypothesized that the opening of large-conductance Ca2+ activated K+ (BKCa) channels may indirectly modulate EC hyperpolarization and nitric oxide (NO) release via myoendothelial gap junctions (MEGJ). To address this hypothesis ‘in situ’ EC ion current recordings, isolated VSMC patch clamp recordings, and simultaneous measurements of NO concentration and relaxation were conducted using segments of the rat superior mesenteric artery. In arteries constricted by α1-adrenoceptor activation, ACh (1μM) evoked EC outward currents, vasorelaxation, and NO release. In contrast to preincubation with iberiotoxin (IbTx, 100nM) application of IbTx after ACh decreased EC outward currents, NO release and vasorelaxation. Furthermore, in phenylephrine (Phe)-contracted arteries treated with a gap junction uncoupler, cabenoxolone (CBX), IbTx failed to decrease ACh-evoked EC outward currents. In addition, CBX decreased EC outward currents, time constant of the capacitative transients, input capacitance, and increased input resistance. In isolated VSMC CBX did not affect BKCa currents. Immunohistochemistry revealed only BKCa channel positive staining in the VSMC layer. Therefore, the present results suggest that BKCa channels are expressed in the VSMC, and that Phe by activation of VSMC BKCa channels modulates ACh-evoked EC outward currents, NO release and vasorelaxation via MEGJ in rat superior mesenteric artery.
Item Description:Available online: 22 December 2011
Im Titel sind 2+ und + hochgestellt
Gesehen am 13.08.2018
Physical Description:Online Resource
ISSN:1090-2104
DOI:10.1016/j.bbrc.2011.12.076

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