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Am J Physiol Heart Circ Physiol 277: H770-H776, 1999;
0363-6135/99 $5.00
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Vol. 277, Issue 2, H770-H776, August 1999

Gene transfer of endothelial nitric oxide synthase (eNOS) in eNOS-deficient mice

Kristy D. Lake-Bruse1, Frank M. Faraci1, Edward G. Shesely2, Nobuyo Maeda3, Curt D. Sigmund1
Donald D. Heistad1
(With the Technical Assistance of Kara L. Brown)

1 Departments of Internal Medicine, Pharmacology, and Physiology, Cardiovascular Center and Center on Aging, University of Iowa College of Medicine, Iowa City, Iowa, 52242; 2 Division of Hypertension and Vascular Research, Henry Ford Hospital, Detroit, Michigan 48202; and 3 Department of Pathology and Laboratory Medicine, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, 27599

Relaxation to acetylcholine (ACh) and calcium ionophore (A-23187) is absent in aortas from endothelial nitric oxide synthase (eNOS)-deficient (eNOS -/-) mice. We hypothesized that gene transfer of eNOS would restore relaxation to ACh and A-23187 in eNOS -/- mice. Aortic rings from eNOS -/- and eNOS +/+ mice were exposed in vitro to vehicle or adenoviral vectors encoding beta -galactosidase (lacZ) or eNOS. Histochemical staining for beta -galactosidase and eNOS demonstrated transduction of endothelial cells and adventitia. Vehicle-treated vessels from eNOS -/- mice did not relax to ACh or A-23187 compared with eNOS +/+ mice. In contrast, relaxation to nitroprusside (NP) was significantly greater in eNOS -/- mice than in eNOS +/+ mice. Gene transfer of eNOS, but not lacZ, to vascular rings of eNOS -/- mice restored relaxation to ACh and A-23187. In vessels from eNOS -/- mice that were transduced with eNOS, Nomega -nitro-L-arginine (10-4 M) inhibited relaxation to ACh and A-23187 but not NP. Thus vascular function can be significantly improved by gene transfer in vessels where a major relaxation mechanism is genetically absent.

adenovirus; aorta; knockout mice


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