Exogenous nitric oxide inhibits proliferation of cultured vascular endothelial cells.
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.
Yang
W
W
Department of Cardiovascular Biomechanics, Faculty of Medicine, University of Tokyo, Japan.
Ando
J
J
Korenaga
R
R
Toyo-oka
T
T
Kamiya
A
A
D000818:Animals; D002417:Cattle; D002455:Cell Division / Q000187:drug effects*; D002478:Cells, Cultured; D006152:Cyclic GMP / Q000031:analogs & derivatives / Q000494:pharmacology / Q000502:physiology; D004247:DNA / Q000096:biosynthesis; D004622:Embryo, Mammalian; D004730:Endothelium, Vascular / Q000166:cytology* / Q000187:drug effects*; D006162:Guanylate Cyclase / Q000037:antagonists & inhibitors; D008751:Methylene Blue / Q000494:pharmacology; D009569:Nitric Oxide / Q000494:pharmacology*; D005996:Nitroglycerin / Q000494:pharmacology; D009599:Nitroprusside / Q000494:pharmacology; D013936:Thymidine / Q000378:metabolism
D009599:Nitroprusside; C016276:8-bromocyclic GMP; D009569:Nitric Oxide; D004247:DNA; D006162:Guanylate Cyclase; D005996:Nitroglycerin; D006152:Cyclic GMP; D008751:Methylene Blue; D013936:Thymidine