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- W2133162144 abstract "Abstract Vascular smooth muscle cells of rat aorta express imidazoline receptors whose stimulation, by drugs or an endogenous ligand, agmatine, inhibits serum-stimulated proliferation. We investigated whether imidazoline receptors are expressed in human vascular smooth muscle cells if their stimulation is antiproliferative. Cultured human coronary artery vascular smooth muscle cells express a nonadrenergic binding site for 3 H-idazoxan and an imidazoline receptor–binding protein as revealed by immunocytochemical and immunoblot analyses with a specific antibody. Idazoxan and agmatine dose-dependently inhibited serum-stimulated proliferation of these cells as measured by the incorporation of 3 H-thymidine (IC 50 : 5 and 70 μmol/L, respectively) and serum-stimulated expression of proliferating cell nuclear antigen and cell numbers. The agents inhibited proliferation of human and rat (aorta) smooth muscle cells stimulated by either norepinephrine (6560±440 disintegrations per minute norepinephrine versus 3345±220 norepinephrine and idazoxan), angiotensin II (7680±335 disintegrations per minute angiotensin II versus 3769±450 angiotensin II and idazoxan), or platelet-derived growth factor (IC 50 : 3 μmol/L for idazoxan and 40 μmol/L for agmatine), indicating inhibition of mitosis mediated by G-protein or receptor tyrosine kinase pathways. We conclude that human vascular smooth muscle cells express imidazoline-receptors whose activation inhibits proliferation by interacting at a distal step in an intracellular signal cascade common to G-protein and receptor tyrosine kinase mitogenic pathways. Agmatine, synthesized in endothelium, may act as a paracrine regulator of vascular smooth muscle cell proliferation through imidazoline receptors, and agents acting at this site may be useful in treating vascular hyperplasia." @default.
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- W2133162144 date "1997-08-01" @default.
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- W2133162144 title "Stimulation of Imidazoline Receptors Inhibits Proliferation of Human Coronary Artery Vascular Smooth Muscle Cells" @default.
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- W2133162144 doi "https://doi.org/10.1161/01.hyp.30.2.295" @default.
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