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Inhibition of neuropeptide Y‐induced potentiation of noradrenaline‐induced vasoconstriction by PP56 ( d ‐ myo ‐inositol 1,2,6‐tris‐phosphate)
Author(s) -
Adamsson M.,
Fallgren B.,
Edvinsson L.
Publication year - 1992
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 - 10.1111/j.1476-5381.1992.tb14216.x
Subject(s) - vasoconstriction , endocrinology , medicine , neuropeptide y receptor , contraction (grammar) , histamine , inositol , chemistry , long term potentiation , mesenteric arteries , vasoconstrictor agents , neuropeptide , inositol phosphate , femoral artery , biology , artery , receptor
1 Although neuropeptide Y (NPY) is a potent vasoconstrictor in many vascular beds, nanomolar concentrations of this peptide potentiate the noradrenaline‐induced contractions in rabbit gastroepiploic and femoral arteries, and guinea‐pig mesenteric and uterine arteries. 2 The potentiating effect of NPY on noradrenaline‐induced contraction was present in endothelium‐denuded femoral arteries. 3 The potentiating effect of NPY on noradrenaline‐induced contraction was antagonized by PP56 ( d ‐ myo ‐inositol 1,2,6‐trisphosphate) in low concentrations (down to 0.1 n m ). This antagonistic effect was observed in all four types of vessels studied. Contractions induced by noradrenaline, histamine, endothelin‐1 and potassium were not altered by PP56 in concentrations upto 1 μ m in femoral artery of rabbit. 4 We provide evidence that a non‐peptide (PP56) can selectively antagonize NPY‐induced effects in rabbit and guinea‐pig peripheral arteries without affecting the vasoconstrictor response to noradrenaline.