(Hypertension. 1997;29:65.)
© 1997 American Heart Association, Inc.
Research Articles (Issue 1, Part 1) |
Endothelin-1 Inhibits Nitric Oxide Synthesis in Vascular Smooth Muscle Cells
the Department of Cardiology, Jichi Medical School, Minamikawachi, Tochigi, Japan.
Correspondence to Uichi Ikeda, MD, PhD, Department of Cardiology, Jichi Medical School, Minamikawachi-Machi, Tochigi 329-04, Japan. E-mail uikeda@jichi.ac.jp
We investigated the effects of endothelin-1 on nitric oxide synthesis in vascular smooth muscle cells. We measured the production of nitrite, a stable metabolite of nitric oxide, and the expression of inducible nitric oxide synthase mRNA and protein in cultured rat vascular smooth muscle cells. Incubation of the cultures with interleukin-1ß (10 ng/mL) for 24 hours caused a significant increase in nitrite production. Endothelin-1 significantly decreased the interleukin-1ß–induced nitrite production by vascular smooth muscle cells in a dose-dependent manner (10-11 to 10-8 mol/L). Incubation with interleukin-1ß for 24 hours induced expression of inducible nitric oxide synthase mRNA and protein in vascular smooth muscle cells, whereas endothelin-1 showed a suppressive effect on their expressions. Addition of the endothelin type A receptor antagonist BQ-485, but not the endothelin type B receptor antagonist BQ-788, dose-dependently inhibited the effect of endothelin-1. After protein kinase C activity was functionally depleted by treatment of cells with phorbol 12-myristate 13-acetate for 24 hours, the effect of endothelin-1 was abolished. These results indicate that endothelin-1 acts on endothelin type A receptors and inhibits nitric oxide synthesis in interleukin-1ß–stimulated vascular smooth muscle cells at least partially through a protein kinase C–dependent pathway.
Key Words: interleukin-1 • nitrites • nitric-oxide synthase • muscle, smooth
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