Abstract-The role of oxidative stress in the long-term regulation of arterial pressure, renal hemodynamics, and renal damage was studied in Dahl salt-sensitive rats. Twenty-eight Dahl S/Rapp strain rats, equipped with indwelling arterial and venous catheters, were subjected to a 3-week intravenous infusion of either low Na (0.9 mmol/d) or high Na (20.6 mmol/d) or the superoxide dismutase mimetic, 4-hydroxyl-2,2,6,6-tetramethylpiperidine-1-oxyl (Tempol), at 125 mol · kg Ϫ1 · h Ϫ1 plus low Na or high Na. After 21 days, mean arterial pressure was 140Ϯ3 mm Hg in the high-Na group, 118Ϯ1 mm Hg (PϽ0.05) in the high-Na/Tempol group, and unchanged in the low-Na/Tempol and low-Na groups. Tempol did not change renal blood flow, glomerular filtration rate, or glomerular cross-sectional area in rats subjected to the high-Na intake but did decrease urinary protein excretion, the percentage of sclerotic glomeruli, and the kidney weight to body weight ratio. In 15 additional Dahl S rats subjected to high or low Na intake for 3 weeks, renal cortical and medullary O 2 · Ϫ release increased significantly in the high-Na group when compared with the low-Na group. Tempol decreased both renal cortical and medullary O 2 · Ϫ release in the high-and low-Na rats, but the decrease in O 2 · Ϫ release was greater in high-Na rats. The data suggest that oxidative stress contributes to Dahl salt-sensitive hypertension and the accompanying renal damage. Key Words: arterial pressure Ⅲ renal disease Ⅲ urine Ⅲ glomerulosclerosis Ⅲ oxidative stress R eactive oxygen species, including superoxide anions (O 2 ·Ϫ ), hydroxyl radicals, and hydrogen peroxide (H 2 O 2 ), have been found in pathological conditions such as atherosclerosis, diabetes, renal disease, and hypertension. O 2 ·Ϫ and H 2 O 2 production by polymorphonuclear leukocytes and the plasma level of lipid peroxides were higher in uncontrolled hypertensive patients than in controls. 1 After blood pressure was reduced in these patients, free-radical generation and lipid peroxide levels returned to normal values. 1 Hypertensive subjects have been shown to have lower levels of the endogenous antioxidants serum ascorbic acid and serum thiols, which might reflect greater consumption of antioxidants. 2 Oxidative stress has also been shown to be involved in hypertensive animal models. The spontaneous hypertensive rat (SHR) is characterized by increased oxidative stress, as demonstrated by the increased O 2 ·Ϫ production in mesenteric arterioles of the SHR. 3,4 In the stroke-prone SHR, O 2 ·Ϫ generation in abdominal aortic tissue was increased compared with their Wistar-Kyoto counterparts. 5 Swei et al 6,7 found enhanced production of superoxide radicals in the microvessels of the mesentery, and plasma H 2 O 2 concentration was increased in hypertensive Dahl salt-sensitive (S) rats compared with Dahl salt-resistant (R) rats. Yet whether increased O 2 ·Ϫ generation contributes to the salt-induced hypertension in the Dahl S rat is not known.Hypertension induces important functional and structural alte...

The roles of oxidative stress and renal superoxide dismutase (SOD) levels and their association with renal damage were studied in Dahl salt-sensitive (S) and salt-resistant (R)/Rapp strain rats during changes in Na intake. After 3 wk of a high (8%)-Na diet in S rats, renal medullary Cu/Zn SOD was 56% lower and Mn SOD was 81% lower than in R high Na-fed rats. After 1, 2, and 3 wk of high Na, urinary excretion of F(2)-isoprostanes, an index of oxidative stress, was significantly greater in S rats compared with R rats. Plasma F(2)-isoprostane concentration increased in the 2-wk S high Na-fed group. After 3 wk, renal cortical and medullary superoxide production was significantly increased in Dahl S rats on high Na intake, and urinary protein excretion, an index of renal damage, was 273 +/- 32 mg/d in S high Na-fed rats and 35 +/- 4 mg/d in R high Na-fed rats (P < 0.05). In conclusion, salt-sensitive hypertension in the S rat is accompanied by marked decreases in renal medullary SOD and greater renal oxidative stress and renal damage than in R rats.

Here we report the incidence of thoracolumbar fracture in blunt trauma and the spectrum of associated injuries. To our knowledge, this paper provides the first epidemiological road map for blunt trauma thoracolumbar injuries.

The norepinephrine transporter (NET ) is a site of action for tricyclic antidepressant drugs and for drugs of abuse such as amphetamine and cocaine. In this study, the binding of [ 3 H]nisoxetine to NETs in the noradrenergic cell group, the locus coeruleus, and the serotonergic cell groups, the dorsal raphe nuclei, was measured autoradiographically in postmortem human brain. 3 H]nisoxetine binding to NETs in monoaminergic nuclei was assessed by measuring the inhibition of its binding by desipramine, imipramine, or citalopram. The order of affinities of these drugs was identical in the locus coeruleus and dorsal and median raphe and was characteristic of binding to NETs (desipramine Ͼ imipramine Ͼ citalopram). Thus, high levels of NETs and an uneven distribution of NETs occur in the locus coeruleus as well as in the dorsal raphe nuclei of the human.