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...

We describe the first use of cinacalcet as monotherapy for severe hypercalcemia in a newborn with NSHPT. The rapid and durable response to cinacalcet suggests that a trial of calcimimetic therapy should be considered early in the course of NSHPT.

The results can guide creation of an initial item pool for a multidimensional profile of HCT outcomes.

Ultrasonography is useful for the evaluation of thyroid nodules, but we found no combination of ultrasound features sufficient to exclude thyroid cancer without a biopsy.