Endothelin-1 Enhances Nitric Oxide–Induced Cytotoxicity in Vascular Smooth Muscle

Hypertension ◽  
1995 ◽  
Vol 25 (4) ◽  
pp. 744-747 ◽  
Author(s):  
Takeshi Nakahashi ◽  
Keisuke Fukuo ◽  
Takuo Inoue ◽  
Shigeto Morimoto ◽  
Shigeki Hata ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
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.

Nitric Oxide Relaxes the Vascular Smooth Muscle Independently of Endothelin-1- and U46619-Induced Intracellular Increase of Calcium

2000 ◽  
Vol 36 (Supplement 1) ◽  
pp. S110-S116 ◽  
Author(s):  
Ghassan Bkaily ◽  
Hadia Shbaklo ◽  
Magda Taoudi-Benchekroun ◽  
Sawsan Sader ◽  
Martine Duval ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Endothelin 1

Nitric Oxide Relaxes the Vascular Smooth Muscle Independently of Endothelin-1- and U46619-Induced Intracellular Increase of Calcium

2000 ◽  
Vol 36 ◽  
pp. S110-S116
Author(s):  
Ghassan Bkaily ◽  
Hadia Shbaklo ◽  
Magda Taoudi-Benchekroun ◽  
Sawsan Sader ◽  
Martine Duval ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Endothelin 1

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

Thrombin Prevents the Expression of Inducible Nitric Oxide Synthase in Vascular Smooth Muscle Cells by a Proteolytically-Activated Thrombin Receptor

1995 ◽  
Vol 74 (03) ◽  
pp. 980-986 ◽  
Author(s):  
Valérie B Schini-Kerth ◽  
Beate Fißithaler ◽  
Thomas T Andersen ◽  
John W Fenton ◽  
Paul M Vanhoutte ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Inducible Nitric Oxide Synthase ◽  
Muscle Cells ◽  
Thrombin Receptor ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

SummaryProteolytically active forms of thrombin (α- and γ-thrombin) and thrombin receptor peptides inhibited the release of nitrite, a stable endproduct of nitric oxide, evoked by interleukin-1 β(IL-1 β) in cultured vascular smooth muscle cells while proteolytically inactive forms [D-Phe-Pro-Arg chloromethyl ketone-α-thrombin (PPACK-α- thrombin) and diisopropylphosphoryl-α-thrombin (DIP-α-thrombin)] had either no or only minimal inhibitory effects. Under bioassay conditions, perfusates from columns containing IL-1 β-activated vascular smooth muscle cells or cells treated with IL-1βplus PPACK-α-thrombin relaxed detector blood vessels. These relaxations were abolished by the inhibitor of nitric oxide synthesis, NG-nitro-L arginine. No relaxations were obtained with untreated cells or IL-1 β-treated cells in the presence of α-thrombin. The expression of inducible nitric oxide synthase mRNA and protein in vascular smooth muscle cells by IL-1 β was impaired by α-thrombin. These results demonstrate that thrombin regulates the expression of the inducible nitric oxide synthase at a transcriptional level via the proteolytic activation of the thrombin receptor in vascular smooth muscle cells

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