Mechanisms of Interleukin-1β Regulation of Nitric Oxide Synthase in Cardiac Myocytes

Hypertension ◽  
1996 ◽  
Vol 27 (3) ◽  
pp. 709-714 ◽  
Author(s):  
Margot C. LaPointe ◽  
Jodi R. Sitkins
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Cardiac Myocytes ◽  
Interleukin 1Β ◽  
Oxide Synthase

Vasculoprotective Role of Inducible Nitric Oxide Synthase at Inflammatory Coronary Lesions Induced by Chronic Treatment With Interleukin-1β in Pigs in Vivo

Circulation ◽  
1997 ◽  
Vol 96 (9) ◽  
pp. 3104-3111 ◽  
Author(s):  
Yoshihiro Fukumoto ◽  
Hiroaki Shimokawa ◽  
Toshiyuki Kozai ◽  
Toshiaki Kadokami ◽  
Kouichi Kuwata ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Inducible Nitric Oxide Synthase ◽  
Chronic Treatment ◽  
Interleukin 1Β ◽  
Coronary Lesions ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

scholarly journals INTERLEUKIN-1β INDUCES NITRIC OXIDE SYNTHASE BY HAMSTER PANCREAS β CELL LINE (HIT-T15)

1993 ◽  
Vol 14 (2) ◽  
pp. 117-122 ◽  
Author(s):  
KAZUKI OHTA ◽  
YUKIO HIRATA ◽  
TAIHEI IMAI ◽  
FUMIAKI MARUMO
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Cell Line ◽  
Interleukin 1Β ◽  
Β Cell ◽  
Oxide Synthase

Endothelin-1 ameliorates contractile depression by lipopolysaccharide in cardiac myocytes

1997 ◽  
Vol 273 (3) ◽  
pp. H1403-H1407 ◽  
Author(s):  
S. Yasuda ◽  
W. Y. Lew
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Cardiac Myocytes ◽  
Contractile Function ◽  
Adult Rabbit ◽  
Nitric Oxide Synthase Inhibitor ◽  
Endothelin 1 ◽  
Cardiac Depression ◽  
Synthase Inhibitor ◽  
Oxide Synthase

Lipopolysaccharide (LPS) induces cardiac depression by activating nitric oxide pathways to increase guanosine 3',5'-cyclic monophosphate (cGMP), a second messenger of nitric oxide. Endothelin-1 (ET-1) may interact with nitric oxide pathways. We hypothesized that ET-1 modulates LPS-induced contractile depression in cardiac myocytes. Adult rabbit cardiac myocytes exposed to LPS (10 ng/ml) developed decreased cell shortening after 6 h, with an increase in cardiac cGMP levels [606 +/- 36 (SE) fmol/mg protein] compared with control myocytes (360 +/- 26 fmol/mg protein, P < 0.05). LPS effects were completely blocked by coincubation with the nitric oxide synthase inhibitor NG-monomethyl-L-arginine (1 mM). Coincubation with ET-1 (10 nM) attenuated the contractile depression and increase in cGMP with LPS (482 +/- 28 fmol/mg protein, P < 0.05 vs. LPS alone). ET-1 alone did not alter cGMP levels (350 +/- 30 fmol/mg protein). ET-1 effects on contractile function were blocked by BQ-123 (10 microM), a selective ET-1 type A receptor antagonist. We conclude that ET-1 ameliorates LPS-induced contractile depression in cardiac myocytes by attenuating LPS effects on nitric oxide-cGMP pathways.

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