Abstract
We demonstrated that angiotensin II (Ang II, 10–1000 nM) induced proliferation of cultured rabbit gingival fibroblasts in a concentration-dependent manner. The Ang II-induced proliferation was inhibited by CV-11974 (AT 1 antagonist; 1 μM) and saralasin (AT 1/AT 2 antagonist; 1 μM), but not by PD123,319 (AT 2 antagonist; 1 μM), suggesting that Ang II-induced proliferation was mediated via AT 1 receptors present in and/or on gingival fibroblasts. The results of Western blot analysis indicated the presence of AT 1 and AT 2 receptors in/on the fibroblasts. In a subsequent radioligand binding assay, the binding of [ 3H]Ang II to the fibroblasts was specific and saturable with both high- and low-affinity sites. Competition binding experiments indicated that Ang II completely displaced [ 3H]Ang II binding, and CV-11974 and PD123,319 maximally displaced up to approximately 63% and 37% of the total binding, respectively. Ang II and CV-11974 completely displaced the [ 3H]DuP753 binding but PD123,319 did not, indicating a single population of binding site. These findings demonstrate that gingival fibroblasts contain both AT 1 and AT 2 receptor subtypes for Ang II, and support that Ang II stimulation of AT 1 receptors results in proliferation of the fibroblasts.
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