Abstract
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.
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