| First Author | Lake-Bruse KD | Year | 1999 |
| Journal | Am J Physiol | Volume | 277 |
| Issue | 2 Pt 2 | Pages | H770-6 |
| PubMed ID | 10444505 | Mgi Jnum | J:56870 |
| Mgi Id | MGI:1342841 | Doi | 10.1152/ajpheart.1999.277.2.H770 |
| Citation | Lake-Bruse KD, et al. (1999) Gene transfer of endothelial nitric oxide synthase (eNOS) in eNOS-deficient mice. Am J Physiol 277(2 Pt 2):H770-6 |
| abstractText | 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, N(omega)-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. |
