ATP-Dependent inhibition of Ca2+-activated K+ channels in vascular smooth muscle cells by neuropeptide Y

1995 ◽  
Vol 431 (1) ◽  
pp. 110-116 ◽  
Author(s):  
Zhigang Xiong ◽  
Donald W. Cheung
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Neuropeptide Y ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
K Channels ◽  
Dependent Inhibition

Neuropeptide Y induced increase of cytosolic and nuclear Ca2+ in heart and vascular smooth muscle cells

2000 ◽  
Vol 78 (2) ◽  
pp. 162-172 ◽  
Author(s):  
Danielle Jacques ◽  
Sawsan Sader ◽  
Nesrine El-Bizri ◽  
Sanaa Chouffani ◽  
Ghada Hassan ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Neuropeptide Y ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells

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.

Neuropeptide Y stimulates DNA synthesis in human vascular smooth muscle cells through neuropeptide Y Y1 receptors

2000 ◽  
Vol 78 (3) ◽  
pp. 256-259 ◽  
Author(s):  
T Nilsson ◽  
L Edvinsson
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Dna Synthesis ◽  
Neuropeptide Y ◽  
Vascular Smooth Muscle Cells ◽  
Thymidine Incorporation ◽  
Muscle Cells ◽  
Dependent Manner ◽  
Mitogenic Effect

We investigated the mitogenic effect, measured as [3H]thymidine incorporation, of neuropeptide Y (NPY) on smooth muscle cells (SMCs) from human subcutaneous arteries (diameter: 0.4 mm). NPY stimulated DNA synthesis in a concentration-dependent manner, Emax 32 ± 5% relative to control. The effect was potently antagonised by the NPY Y1 receptor antagonist BIBP3226 ((R)-N2-(diphenylacetyl)-N-[(4-hydroxy-phenyl)methyl]-D-arginine-amide), indicating the effect to be mediated via the NPY Y1 receptor. Noradrenaline (NA) also induced mitogenesis, Emax 35 ± 10% relative to control. When added together, NPY and NA potentiated the [3H]thymidine incorporation, Emax 109 ± 38% relative to control. Also, this effect seems to be mediated by the NPY Y1 receptor, since BIBP3226 blocked the effect (44 ± 9% relative to control). The mitogenic effect of NPY and NA, two important transmitters of the sympathetic nervous system, might have clinical consequences on conditions with elevated sympathetic nerve activity.Key words: BIBP3226, mitogenesis, neuropeptide Y, vascular smooth muscle cells.

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