Neuropeptide Y receptor-effector coupling mechanisms in cultured vascular smooth muscle cells.
Primary cultures of rabbit pulmonary artery (RPA) vascular smooth muscle (VSM) were utilized to determine the coupling of neuropeptide Y (NPY) receptors to several effector systems in VSM. NPY inhibited forskolin-stimulated adenylate cyclase by 65%, with an EC50 of 0.3 nM. However, NPY did not stimulate phosphoinositide (PI) hydrolysis or the elevation of cytosolic calcium, (Ca+2)i, in cultured RPA-VSM cells, nor did it potentiate norepinephrine-induced PI hydrolysis or elevation of (Ca+2)i. These results suggest that NPY-induced vasocontraction is not mediated by PI hydrolysis or the modulation of (Ca+2)i.
Reynolds
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Dept. Heart and Hypertension Research, Cleveland Clinic Foundation, OH 44106.
Yokota
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D000818:Animals; D002118:Calcium / Q000378:metabolism; D002478:Cells, Cultured; D005576:Colforsin / Q000494:pharmacology; D000242:Cyclic AMP / Q000378:metabolism; D003600:Cytosol / Q000378:metabolism; D007295:Inositol Phosphates / Q000096:biosynthesis; D007700:Kinetics; D009131:Muscle, Smooth, Vascular / Q000378:metabolism*; D009478:Neuropeptide Y / Q000378:metabolism* / Q000494:pharmacology; D011651:Pulmonary Artery / Q000378:metabolism; D011817:Rabbits; D017476:Receptors, Neuropeptide Y; D017981:Receptors, Neurotransmitter / Q000378:metabolism*
D007295:Inositol Phosphates; D009478:Neuropeptide Y; D017476:Receptors, Neuropeptide Y; D017981:Receptors, Neurotransmitter; D005576:Colforsin; D000242:Cyclic AMP; D002118:Calcium