Recombinant Nitric Oxide Synthase Gene Transfer: Potential Roles in Gene Therapy of Cerebrovascular Disease

2001 ◽  
pp. 142-147
Author(s):  
Alex F. Chen ◽  
Zvonimir S. Katusic
Keyword(s):  
Nitric Oxide ◽  
Gene Therapy ◽  
Nitric Oxide Synthase ◽  
Gene Transfer ◽  
Cerebrovascular Disease ◽  
Oxide Synthase ◽  
Transfer Potential

Adventitial Gene Transfer of Recombinant Endothelial Nitric Oxide Synthase to Rabbit Carotid Arteries Alters Vascular Reactivity

Circulation ◽  
1997 ◽  
Vol 96 (7) ◽  
pp. 2254-2261 ◽  
Author(s):  
Iftikhar J. Kullo ◽  
Geza Mozes ◽  
Robert S. Schwartz ◽  
Peter Gloviczki ◽  
Thomas B. Crotty ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Gene Transfer ◽  
Endothelial Nitric Oxide Synthase ◽  
Vascular Reactivity ◽  
Carotid Arteries ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Nitric oxide synthase gene therapy: progress and prospects

2009 ◽  
Vol 9 (7) ◽  
pp. 867-878 ◽  
Author(s):  
Deirdre M O'Connor ◽  
Timothy O'Brien
Keyword(s):  
Nitric Oxide ◽  
Gene Therapy ◽  
Nitric Oxide Synthase ◽  
Oxide Synthase

Recombinant Gene Transfer of Endothelial Nitric Oxide Synthase Augments Coronary Artery Relaxations During Hypoxia

Circulation ◽  
1999 ◽  
Vol 100 (suppl_2) ◽  
Author(s):  
David G. Cable ◽  
Vincent J. Pompili ◽  
Timothy O’Brien ◽  
Hartzell V. Schaff
Keyword(s):  
Nitric Oxide ◽  
Coronary Artery ◽  
Nitric Oxide Synthase ◽  
Gene Transfer ◽  
Coronary Arteries ◽  
Endothelial Nitric Oxide Synthase ◽  
No Production ◽  
Viral Control ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Background —Coronary arteries respond to hypoxia with transient relaxations, which increases coronary blood flow, in part, by release of nitric oxide. We hypothesized that increased expression of nitric oxide synthase might further augment blood vessel relaxation during hypoxia. The present study examined the effect of adenovirus-mediated transfer of bovine endothelial nitric oxide synthase (eNOS) on hypoxia-induced transient relaxations in canine coronary arteries. Methods and Results —Paired segments of coronary arteries were exposed to vehicle (phosphate-buffered saline with albumin) or an adenovirus encoding either E coli β-galactosidase (Ad.CMVLacZ, viral control; 10 10 pfu/mL) or eNOS (Ad.CMVeNOS; 10 10 pfu/mL) for 2 hours at 37°C. Immunohistochemistry with a monoclonal antibody specific for eNOS documented both endothelial and adventitial expression in Ad.CMVeNOS arteries, whereas vehicle and viral controls demonstrated only constitutive expression. Levels of cGMP were increased 5-fold in Ad.CMVeNOS arteries compared with controls. In arteries exposed to Ad.CMVeNOS, maximum contraction to prostaglandin F 2α was reduced compared with viral controls, and this effect was eliminated by pretreatment with a competitive inhibitor of eNOS ( N G -monomethyl- l -arginine, 10 −3 mol/L). Hypoxia-induced transient relaxation (95% N 2 -5% CO 2 ) in Ad.CMVeNOS arteries (45.2±8.8%, n=6) was augmented compared with vehicle (26.3±6.0%) or viral (27.2±7.1%) controls. Conclusions —Adenovirus-mediated gene transfer of nitric oxide synthase reduces receptor-dependent contractions and augments hypoxia-induced relaxations in canine coronary arteries; this method of augmentation of NO production might be advantageous for reduction of coronary artery vasospasm.

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