β-Adrenergic modulation of maxi-K channels in vascular smooth muscle via G i through a membrane-delimited pathway

1999 ◽  
Vol 437 (3) ◽  
pp. 508-510 ◽  
Author(s):  
Sungkwon Chung ◽  
Heun Soh ◽  
D.-Y. Uhm
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
K Channels ◽  
Adrenergic Modulation

Involvement of K+ channels in the relaxant effects of YC-1 in vascular smooth muscle

1999 ◽  
Vol 382 (1) ◽  
pp. 11-18 ◽  
Author(s):  
Sabine Seitz ◽  
Jörg W Wegener ◽  
Johanna Rupp ◽  
Makino Watanabe ◽  
Andreas Jost ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
K Channels

scholarly journals EDHF: an update

2009 ◽  
Vol 117 (4) ◽  
pp. 139-155 ◽  
Author(s):  
Michel Félétou ◽  
Paul M. Vanhoutte
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Electrical Coupling ◽  
Muscle Cells ◽  
Therapeutic Interventions ◽  
K Channels ◽  
Acid Metabolites

The endothelium controls vascular tone not only by releasing NO and prostacyclin, but also by other pathways causing hyperpolarization of the underlying smooth muscle cells. This characteristic was at the origin of the term ‘endothelium-derived hyperpolarizing factor’ (EDHF). However, this acronym includes different mechanisms. Arachidonic acid metabolites derived from the cyclo-oxygenases, lipoxygenases and cytochrome P450 pathways, H2O2, CO, H2S and various peptides can be released by endothelial cells. These factors activate different families of K+ channels and hyperpolarization of the vascular smooth muscle cells contribute to the mechanisms leading to their relaxation. Additionally, another pathway associated with the hyperpolarization of both endothelial and vascular smooth muscle cells contributes also to endothelium-dependent relaxations (EDHF-mediated responses). These responses involve an increase in the intracellular Ca2+ concentration of the endothelial cells, followed by the opening of SKCa and IKCa channels (small and intermediate conductance Ca2+-activated K+ channels respectively). These channels have a distinct subcellular distribution: SKCa are widely distributed over the plasma membrane, whereas IKCa are preferentially expressed in the endothelial projections toward the smooth muscle cells. Following SKCa activation, smooth muscle hyperpolarization is preferentially evoked by electrical coupling through myoendothelial gap junctions, whereas, following IKCa activation, K+ efflux can activate smooth muscle Kir2.1 and/or Na+/K+-ATPase. EDHF-mediated responses are altered by aging and various pathologies. Therapeutic interventions can restore these responses, suggesting that the improvement in the EDHF pathway contributes to their beneficial effect. A better characterization of EDHF-mediated responses should allow the determination of whether or not new drugable targets can be identified for the treatment of cardiovascular diseases.

PCR-based analysis of voltage-gated K+ channels in vascular smooth muscle

1995 ◽  
Vol 145 (1) ◽  
pp. 39-44 ◽  
Author(s):  
Peter Zahradka ◽  
Karen D. Harris ◽  
Barbara Triggs-Raine ◽  
Ginette Lamontagne ◽  
Normand Leblanc
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
K Channels ◽  
Voltage Gated

Daidzein relaxes rat cerebral basilar artery via activation of large-conductance Ca2+-activated K+ channels in vascular smooth muscle cells

2010 ◽  
Vol 630 (1-3) ◽  
pp. 100-106 ◽  
Author(s):  
Hong-Tao Zhang ◽  
Yan Wang ◽  
Xiu-Ling Deng ◽  
Ming-Qing Dong ◽  
Li-Mei Zhao ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Basilar Artery ◽  
Muscle Cells ◽  
K Channels
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