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Extracellular l-arginine Enhances Relaxations Induced by Opening of Calcium-Activated SKCa Channels in Porcine Retinal Arteriole. | LitMetric

AI Article Synopsis

  • The study explored how l-arginine, a substrate for nitric oxide production, affects relaxations in endothelial cells via small conductance calcium-activated potassium channels (SKCa).
  • It found that acetylcholine increases l-arginine uptake, but blocking SKCa and intermediate conductance channels reduces this uptake; a specific transporter blocker, l-lysine, also inhibited l-arginine uptake.
  • The research suggests that SKCa channels play a crucial role in regulating l-arginine uptake through the y+ transporter system, highlighting that enhancing l-arginine delivery in dysfunctional vasculature may require targeting these channels for effective vasodilation.

Article Abstract

We investigated whether the substrate for nitric oxide (NO) production, extracellular l-arginine, contributes to relaxations induced by activating small (SKCa) conductance Ca-activated potassium channels. In endothelial cells, acetylcholine increased H-l-arginine uptake, while blocking the SKCa and the intermediate (IKCa) conductance Ca-activated potassium channels reduced l-arginine uptake. A blocker of the y+ transporter system, l-lysine also blocked H-l-arginine uptake. Immunostaining showed co-localization of endothelial NO synthase (eNOS), SKCa3, and the cationic amino acid transporter (CAT-1) protein of the y+ transporter system in the endothelium. An opener of SKCa channels, cyclohexyl-[2-(3,5-dimethyl-pyrazol-1-yl)-6-methyl-pyrimidin-4-yl]-amine (CyPPA) induced large currents in endothelial cells, and concentration-dependently relaxed porcine retinal arterioles. In the presence of l-arginine, concentration-response curves for CyPPA were leftward shifted, an effect unaltered in the presence of low sodium, but blocked by l-lysine in the retinal arterioles. Our findings suggest that SKCa channel activity regulates l-arginine uptake through the y+ transporter system, and we propose that in vasculature affected by endothelial dysfunction, l-arginine administration requires the targeting of additional mechanisms such as SKCa channels to restore endothelium-dependent vasodilatation.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6515554PMC
http://dx.doi.org/10.3390/ijms20082032DOI Listing

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