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Neuropeptide Y increases 4‐aminopyridine‐sensitive transient outward potassium current in rat ventricular myocytes
Author(s) -
Heredia M P,
FernándezVelasco M,
Benito G,
Delgado C
Publication year - 2002
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1038/sj.bjp.0704643
Subject(s) - cardiac transient outward potassium current , 4 aminopyridine , myocyte , potassium channel , chemistry , medicine , potassium , transient (computer programming) , neuropeptide y receptor , current (fluid) , endocrinology , electrophysiology , biophysics , patch clamp , biology , neuropeptide , physics , receptor , organic chemistry , computer science , thermodynamics , operating system
The modulation of 4‐aminopyridine sensitive transient outward potassium current (4‐AP I to ) by neuropeptide Y (NPY) (100 n M ) in rat ventricular myocytes was examined using the whole cell voltage‐clamp technique. Continuous exposure to NPY (100 n M ) for 3 – 6 h significantly increased 4‐AP I to density. The stimulation of 4‐AP I to density by NPY was concentration‐dependent (EC 50 =10 n M ). In the presence of BIBP 3226, an NPY receptor antagonist that binds selectively to NPY Y1‐receptors, the effect of NPY on 4‐AP I to density was maintained. However, in the presence of BIIE 0246, a highly selective non‐peptide NPY Y2‐receptor antagonist, NPY was unable to increase 4‐AP I to density. The effect of NPY on 4‐AP I to density was prevented by pretreatment with 500 ng ml −1 pertussis toxin (PTX) and by the specific protein kinase C (PKC) inhibitor, calphostin C (100 n M ). Thus, short term exposure to NPY induces an increase of 4‐AP I to density in rat ventricular myocytes mediated by Y2‐receptors and involving the action of PKC via a PTX‐sensitive signalling cascade.British Journal of Pharmacology (2002) 135 , 1701–1706; doi: 10.1038/sj.bjp.0704643

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