ArticlePflugers Archiv : European journal of physiology1994
Neuropeptide Y inhibits Ca(2+)-activated K+ channels in vascular smooth muscle cells from the rat tail artery.
Article in Pflugers Archiv : European journal of physiology, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 15 citations in OpenAlex.
- BKCa and KV channels limit conducted vasomotor responses in rat mesenteric terminal arterioles.Pflugers Archiv : European journal of physiology · 2012Article
- NPY receptors as potential targets for anti-obesity drug development.British journal of pharmacology · 2011Article
- Interactions between neuropeptide Y and the adenylate cyclase pathway in rat mesenteric small arteries: role of membrane potential.The Journal of physiology · 1997Article
- Neuropeptide Y modulates ATP-induced increases in internal calcium via the adenylate cyclase/protein kinase A system in a human neuroblastoma cell line.The Biochemical journal · 1997Article
- Synthesis and characterization of a selective peptide antagonist of neuropeptide Y vascular postsynaptic receptors.British journal of pharmacology · 1996Article
- ATP-Dependent inhibition of Ca2+-activated K+ channels in vascular smooth muscle cells by neuropeptide Y.Pflugers Archiv : European journal of physiology · 1995Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The effects of neuropeptide Y (NPY) on the Ca(2+)-activated K+ channel in smooth muscle cells from the rat tail artery were studied by whole-cell and single-channel patch-clamp recording techniques. In the presence of nifedipine (1 microM), whole-cell outward currents through Ca(2+)-activated K+ channels were inhibited by NPY in a dose-dependent manner from 20 to 200 nM. A maximum inhibition to about 48% of the control current could be achieved. Recordings from outside-out patches showed that the open probability of Ca(2+)-activated K+ channels were similarly inhibited by NPY. At 200 nM NPY, the open probability was reduced to about 36% of the control value. NPY did not affect the open times or current amplitude, but increased significantly the short (from 0.49 to 0.58 ms) and long (from 441 to 728 ms) closed times. Inhibition of Ca(2+)-activated K+ channels by NPY may contribute to its excitatory action on vascular smooth muscle cells.
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