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VASCULAR SMOOTH MUSCLE CELL PROLIFERATION IN SHR AND WKY RATS: EVIDENCE FOR SPECIFIC DIFFERENCES IN GROWTH INHIBITORY REGULATORY MECHANISMS
Author(s) -
Agrotis Alex,
Bray Paula J.,
Saltis John,
Bobik Alex
Publication year - 1993
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.1993.tb01696.x
Subject(s) - inhibitory postsynaptic potential , vascular smooth muscle , cell growth , endocrinology , medicine , cell , smooth muscle , microbiology and biotechnology , regulator , chemistry , biology , biochemistry , gene
SUMMARY 1. This study examined and compared the actions of transforming growth factor‐β 1 (TGF‐β 1 ), heparin, dexamethasone and interferon‐γ on platelet‐derived growth factor‐BB (PDGF‐BB)‐stimulated proliferation of vascular smooth muscle cells (VSMC) from normotensive, Wistar‐Kyoto (WKY) rats and spontaneously hypertensive rats (SHR). 2. Heparin, dexamethasone and interferon‐γ all inhibited VSMC proliferation stimulated by PDGF‐BB in both SHR and WKY rats. There was no difference ( P >0.05) in their inhibitory effects, which varied between 40 and 85% for the different agents. 3. Similarly, TGF‐β 1 inhibited PDGF‐BB‐stimulated VSMC proliferation in WKY rats by approximately 50%. In contrast, TGF‐β 1 potentiated growth factor action on cell proliferation in the SHR by approximately 40%. 4. Specific TGF‐β 1 ‐stimulated regulatory mechanisms involved in the inhibition of proliferation are absent in SHR and this defect may contribute to the vascular hypertrophy which is apparent in genetic hypertension.