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Articles in PresS, published online ahead of print June 20, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00079.2002
Submitted on January 30, 2002
Accepted on June 17, 2002
1 Internal Medicine, University of Iowa, Iowa City, IA, USA
2 Internal Medicine, University of Iowa, Iowa City, IA, USA; Physiology, University of Iowa, Iowa City, IA, USA
3 Internal Medicine, University of Iowa, Iowa City, IA, USA; Pharmacology, University of Iowa, Iowa City, IA, USA
* To whom correspondence should be addressed. E-mail: frank-faraci{at}uiowa.edu.
Acute elevations in plasma angiotensin II have been associated with elevations in arterial blood pressure and increased superoxide in vessels. The purpose of this study was to examine vascular function and the role of superoxide in mice that chronically express human renin (R+) and human angiotensinogen (A+). Vascular responses of thoracic aorta from R+/A+ mice and from their normotensive littermates (RA- mice) were examined in vitro. Endothelium-dependent relaxation to acetylcholine was impaired in vessels from R+/A+ mice (e.g., maximal relaxation to 100 µM acetylcholine was 45±5% and 65±3% in R+/A+ and RA- mice, respectively; P<0.05). Relaxation was also impaired to the endothelium-independent dilators authentic nitric oxide and nitroprusside in vessels from R+/A+. Although relaxation to submaximal concentrations was impaired, maximal relaxation to the endothelium-independent, non-nitric oxide dilator papaverine was similar in vessels from R+/A+ and RA- mice. Incubation of vessels from R+/A+ mice with 4,5-dihydroxy-1,3-benzene disulfonic acid (Tiron; 1 mM), a superoxide scavenger, significantly improved relaxation to acetylcholine, nitric oxide, and nitroprusside. In contrast, incubation with diethyldithiocarbamate (1 mM), a selective inhibitor of copper-containing superoxide dismutases, significantly reduced acetylcholine- and nitroprusside-induced relaxation in vessels from both R+/A+ and RA- mice. Basal superoxide levels, as measured using lucigenin-enhanced chemiluminscence (5 µM lucigenin) and hydroethidine-based fluorescent confocal microscopy, were higher (P<0.05) in vessels from R+/A+ mice and were Tiron- and polyethylene glycol-superoxide dismutase-sensitive. Incubation of vessels with diphenylene iodonium (100 µM), a selective inhibitor of flavin-containing enzymes including NAD(P)H oxidase, reduced (P<0.05) the lucigenin signal in R+/A+ mice. These results suggest that increased superoxide levels contribute to impaired nitric oxide-mediated relaxation in this genetic model of chronic angiotensin II-dependent hypertension.
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