scholarly journals Endothelin-1 Inhibits Nitric Oxide Synthesis in Vascular Smooth Muscle Cells

Hypertension ◽  
1997 ◽  
Vol 29 (1) ◽  
pp. 65-69 ◽  
Author(s):  
Uichi Ikeda ◽  
Keiji Yamamoto ◽  
Yoshikazu Maeda ◽  
Masahisa Shimpo ◽  
Toshiko Kanbe ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Nitric Oxide Synthesis ◽  
Endothelin 1

Endothelin-1 Enhances Nitric Oxide-Induced Cell Death in Cultured Vascular Smooth-Muscle Cells

1998 ◽  
Vol 31 ◽  
pp. S351-S353 ◽  
Author(s):  
Takeshi Nakahashi ◽  
Keisuke Fukuo ◽  
Hiroyuki Nishimaki ◽  
Shigeki Hata ◽  
Masumi Shimizu ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cell Death ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Endothelin 1

Nitric oxide attenuates endothelin-1-induced activation of ERK1/2, PKB, and Pyk2 in vascular smooth muscle cells by a cGMP-dependent pathway

2007 ◽  
Vol 293 (4) ◽  
pp. H2072-H2079 ◽  
Author(s):  
Ali Bouallegue ◽  
Grace Bou Daou ◽  
Ashok K. Srivastava
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Signaling Pathways ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Cellular Growth ◽  
Dependent Manner ◽  
Endothelin 1

Nitric oxide (NO), in addition to its vasodilator action, has also been shown to antagonize the mitogenic and hypertrophic responses of growth factors and vasoactive peptides such as endothelin-1 (ET-1) in vascular smooth muscle cells (VSMCs). However, the mechanism by which NO exerts its antimitogenic and antihypertrophic effect remains unknown. Therefore, the aim of this study was to determine whether NO generation would modify ET-1-induced signaling pathways involved in cellular growth, proliferation, and hypertrophy in A-10 VSMCs. Treatment of A-10 VSMCs with S-nitroso- N-acetylpenicillamine (SNAP) or sodium nitroprusside (SNP), two NO donors, attenuated the ET-1-enhanced phosphorylation of several key components of growth-promoting and hypertrophic signaling pathways such as ERK1/2, PKB, and Pyk2. On the other hand, inhibition of the endogenous NO generation with NG-nitro-l-arginine methyl ester, a nitric oxide synthase inhibitor, increased the ET-1-induced phosphorylation of these signaling components. Since NO mediates its effect principally through a cGMP-soluble guanylyl cyclase (sGC) pathway, we investigated the role of these molecules in NO action. 8-Bromoguanosine 3′,5′-cyclic monophosphate, a nonmetabolizable and cell-permeant analog of cGMP, exhibited a effect similar to that of SNAP and SNP. Furthermore, 1 H-[1,2,4]oxadiazolo[4,3- a]quinoxalin-1-one (ODQ), an inhibitor of sGC, reversed the inhibitory effect of NO on ET-1-induced responses. SNAP treatment also decreased the protein synthesis induced by ET-1. Together, these data demonstrate that NO, in a cGMP-dependent manner, attenuated ET-1-induced phosphorylation of ERK1/2, PKB, and Pyk2 and also antagonized the hypertrophic effects of ET-1. It may be suggested that NO-induced generation of cGMP contributes to the inhibition of ET-1-induced mitogenic and hypertrophic responses in VSMCs.

PACAP Augments Nitric Oxide Synthesis in Rat Vascular Smooth Muscle Cells Stimulated with IL-1α

2006 ◽  
Vol 921 (1) ◽  
pp. 415-419 ◽  
Author(s):  
HIROFUMI SANO ◽  
ATSURO MIYATA ◽  
KUMI SATO ◽  
HIROYUKI KAIYA ◽  
HISAYUKI MATSUO ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Nitric Oxide Synthesis
Sign in / Sign up

Export Citation Format

Share Document