Hypoxia Upregulates Inducible (Type II) Nitric Oxide Synthase in an HIF-1 Dependent Manner in Rat Pulmonary Microvascular But Not Aortic Smooth Muscle Cells

CHEST Journal ◽  
1998 ◽  
Vol 114 (1) ◽  
pp. 33S-34S ◽  
Author(s):  
Lisa A. Palmer ◽  
Roger A. Johns
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Nitric Oxide Synthase ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Dependent Manner ◽  
Type Ii ◽  
Aortic Smooth Muscle Cells ◽  
Aortic Smooth Muscle ◽  
Oxide Synthase

Induction and cDNA sequence of inducible nitric oxide synthase from canine aortic smooth muscle cells

1998 ◽  
Vol 275 (4) ◽  
pp. H1122-H1129 ◽  
Author(s):  
Xiaofang Wang ◽  
Christopher G. A. McGregor ◽  
Virginia M. Miller
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Nitric Oxide Synthase ◽  
Smooth Muscle Cells ◽  
Allograft Rejection ◽  
Muscle Cells ◽  
Type Ii ◽  
Rt Pcr ◽  
Aortic Smooth Muscle ◽  
Oxide Synthase

An inducible isoform of nitric oxide synthase (type II, iNOS) is expressed in cardiac and vascular smooth muscle in response to inflammatory cytokines. The dog is an important large animal used for cardiovascular research including effects of exercise, heart failure, and allograft rejection. However, molecular probes for iNOS developed in other mammals have not been reliable for the study of iNOS induction in canine vascular smooth muscle. Experiments were designed to develop a molecular probe for canine iNOS. Smooth muscle cells were isolated from canine aortas. The cells ( passages 3–10) were incubated for 1, 3, 6, 12, 24, 48, or 72 h in the absence and presence of Escherichia coli lipopolysaccharide (LPS) to induce iNOS. Total RNA was isolated from the cells using standard techniques. RT-PCR with primers against conserved regions of all known iNOS enzyme was used to clone the iNOS cDNA. RT-PCR showed a single band only from cells treated with LPS. Cloned cDNA from cultured canine aortic smooth muscle cells has 84% homology to human, 81% to rat, and 81% to mouse iNOS gene. Identification of the cDNA for canine iNOS will be useful in the study of differential, transcriptional regulation of inducible (type II) compared with constitutive endothelial (type III) NOS in canine studies of allograft rejection and cardiovascular disease.

Hemin activation of an inducible isoform of nitric oxide synthase in vascular smooth-muscle cells

1995 ◽  
Vol 83 (5) ◽  
pp. 862-866 ◽  
Author(s):  
Satoshi Suzuki ◽  
Neal F. Kassell ◽  
Kevin S. Lee
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Subarachnoid Hemorrhage ◽  
Nitric Oxide Synthase ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Dependent Manner ◽  
Oxide Synthase

✓ Hemin is a prominent breakdown product of hemoglobin, and high levels of hemin are found in the cerebrospinal fluid during subarachnoid hemorrhage—induced vasospasm. The possible role of hemin in modifying vascular function was examined in the present study by testing its effects on nitric oxide synthase (NOS) activity in cultured rat aortic smooth-muscle cells. Nitric oxide synthase activity was estimated from the amounts of accumulated nitrite and nitrate, which are oxidative products of nitric oxide (NO). Hemin (1–100 µM) increased the levels of nitrite and nitrate in culture medium in a dose- and time-dependent manner. The hemin-induced elevation of nitrite and nitrate was inhibited significantly by the NOS inhibitor, Nω-nitro-l-arginine (300 µM), and by the protein synthesis inhibitor, cycloheximide (5 µg/ml). These results indicate that hemin is capable of stimulating the expression of an inducible isoform of NOS (iNOS) in vascular smooth muscle. Transcriptional expression of iNOS is known to cause injurious effects on the maintenance of cellular homeostasis by generating extremely high levels of NO. The generation of hemin from methemoglobin during hemolysis of a subarachnoid blood clot could therefore stimulate an excessive production of NO in vascular smooth-muscle cells. It is postulated that this series of events contributes to the development of vascular injury associated with cerebral vasospasm after aneurysmal subarachnoid hemorrhage.

Thrombin inhibits induction of nitric oxide synthase in vascular smooth muscle cells

1993 ◽  
Vol 264 (2) ◽  
pp. H611-H616
Author(s):  
V. B. Schini ◽  
S. Catovsky ◽  
W. Durante ◽  
T. Scott-Burden ◽  
A. I. Schafer ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Nitric Oxide Synthase ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Rat Aorta ◽  
Thrombin Inhibitor ◽  
Dependent Manner ◽  
Cultured Smooth Muscle Cells ◽  
Oxide Synthase

Experiments were designed to examine whether thrombin affects the production of nitric oxide-like factor(s) evoked by interleukin-1 beta (IL-1 beta) in cultured smooth muscle cells from the rat aorta. IL-1 beta stimulated the release of nitrite (a stable oxidation product of nitric oxide) from cultured smooth muscle cells. Thrombin inhibited in a concentration-dependent manner the release of nitrite caused by IL-1 beta. The inhibition was prevented by hirudin (a thrombin inhibitor) and required the presence of thrombin before or during the induction period. Under bioassay conditions, the perfusates from columns containing IL-1 beta-treated smooth muscle cells relaxed detector rat aortic rings without endothelium. The addition of IL-1 beta-treated smooth muscle cells to suspensions of indomethacin-treated platelets inhibited their aggregation. Control untreated smooth muscle cells or cells treated with thrombin alone did not have such effects. The treatment of smooth muscle cells with IL-1 beta in combination with thrombin blunted both the relaxing activities of the perfusates under bioassay conditions and the inhibition of platelet aggregation. These observations indicate that thrombin inhibits the production of nitric oxide-like factor(s) evoked by the inducible nitric oxide synthase in cultured smooth muscle cells from rat aorta.

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