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Gastrointestinal Research Unit and Anesthesia Research Unit, Mayo Clinic, Rochester, Minnesota 55905
Endothelial nitric oxide synthase
(eNOS)-derived nitric oxide (NO) contributes to hepatic vascular
homeostasis. The aim of this study was to examine whether delivery of
an adenoviral vector encoding eNOS gene to liver affects vasomotor
function in vivo and the mechanism of NO production in vitro. Rats were
administered adenoviruses encoding 
-galactosidase (AdCMVLacZ) or
eNOS (AdCMVeNOS) via tail vein injection and studied 1 wk later. In
animals transduced with AdCMVLacZ, -galactosidase activity was
increased in the liver, most prominently in hepatocytes. In
AdCMVeNOS-transduced animals, eNOS protein levels and catalytic
activity were significantly increased. Overexpression of eNOS
diminished baseline perfusion pressure and constriction in response to
the 
1-agonist methoxamine in the perfused liver.
Transduction of cultured hepatocytes with AdCMVeNOS resulted in the
targeting of recombinant eNOS to a perinuclear distribution and binding
with the NOS-activating protein heat shock protein 90. These events
were associated with increased ionomycin-stimulated NO release. In
summary, this is the first study to demonstrate successful delivery of
the recombinant eNOS gene to liver in vivo and in vitro with ensuing NO production.
hepatic perfusion; adenovirus vector; -galactosidase
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