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      Exogenous nitric oxide inhibits proliferation of cultured vascular endothelial cells.

      Biochemical and Biophysical Research Communications

      Endothelium, Vascular, Cattle, Cell Division, drug effects, Cells, Cultured, Cyclic GMP, analogs & derivatives, pharmacology, physiology, DNA, biosynthesis, Embryo, Mammalian, Animals, cytology, Guanylate Cyclase, antagonists & inhibitors, Methylene Blue, Nitric Oxide, Nitroglycerin, Nitroprusside, Thymidine, metabolism

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          Abstract

          Cultured bovine fatal aortic endothelial cells (BAECs) were stimulated with nitric oxide (NO)-releasing vasodilators and NO gas-saturated solution, and changes in the cell proliferation were examined. Sodium nitroprusside (SNP) and nitroglycerin (NTG) shifted the growth curve downward, and inhibited 3H-thymidine incorporation by the ECs in a dose-dependent manner. Application of NO solution also reduced 3H-thymidine incorporation. SNP, NTG and NO solution increased the intracellular cGMP in BAECs. A cGMP analog, 8-bromo-cGMP, inhibited 3H-thymidine incorporation, and a guanylate cyclase inhibitor, methylene blue, almost completely blocked the inhibitory effect of SNP and NTG on 3H-thymidine incorporation. These findings suggest that exogenous NO inhibits EC proliferation, and that intracellular cGMP is involved in the inhibitory effect of NO.

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          7916569

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