Recent studies have implicated a contribution of oxidative stress to the development of hypertension. Studies were performed to determine the effects of the superoxide dismutase (SOD) mimetic 4-hydroxy-2,2,6,6-tetramethylpiperidine-N-oxyl (Tempol) on vascular superoxide production and renal sympathetic nerve activity (RSNA) in anesthetized Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR). Compared with WKY rats (n=6), SHR showed a doubled vascular superoxide production, which was normalized by treatment with Tempol (3 mmol/L, n=7). In WKY rats (n=6), Tempol (30 mg/kg IV) significantly decreased mean arterial pressure (MAP) from 108+/-5 to 88+/-6 mm Hg and HR from 304+/-9 to 282+/-6 beats/min. In SHR (n=6), Tempol significantly decreased MAP from 166+/-4 to 123+/-9 mm Hg and HR from 380+/-7 to 329+/-12 beats/min. Furthermore, Tempol significantly decreased RSNA in both WKY rats and SHR. On the basis of group comparisons, the percentage decreases in MAP (-28+/-4%), HR (-16+/-3%) and integrated RSNA (-63+/-6%) in SHR were significantly greater than in WKY rats (-17+/-3%, -9+/-2%, and -30+/-4%, respectively). In SHR, changes in integrated RSNA were highly correlated with changes in MAP (r=0.85, P<0.0001) during administration of Tempol (3, 10, and 30 mg/kg IV). In both WKY rats and SHR (n=4, respectively), intracerebroventricular injection of Tempol (300 micro g/1 micro L) did not alter MAP, HR, or RSNA. Intravenous administration of a SOD inhibitor, diethyldithio-carbamic acid (30 mg/kg), significantly increased MAP, HR, and integrated RSNA in both WKY rats and SHR (n=6, respectively). These results suggest that augmented superoxide production contributes to the development of hypertension through activation of the sympathetic nervous system.

In Japanese adults who chose to be screened by a general health checkup system, the prevalence of abnormal thyroid function was nearly 10%. In a high percentage of these patients, abnormal thyroid function could not be detected by their history or physical examination. Just a physical examination without thyroid function tests, particularly serum TSH levels, was not adequate even when performed by a thyroid specialist.

The recent development of contrast echography has made renal enhancement possible through an intravenous injection of microbubble-based contrast. In animal models, tissue perfusion can be quantified using contrast echography by measurement of the rate at which microbubbles replenish tissue after their ultrasound-induced destruction. Our purpose in this study was to evaluate renal blood flow with contrast echography in humans. To increase the sensitivity for microbubbles, we used a combination of power Doppler harmonic and intermittent imaging. The pulsing interval (PI) was changed from 10 cardiac cycles to 1 cardiac cycle during an intravenous infusion of the contrast agent, and alterations in the intensity of the renal cortex were represented as a decline ratio (DR). In 24 patients with various renal diseases, we were able to observe all 48 kidneys with adequate enhancement of the renal cortex. At PI of 10 cardiac cycles, the enhancement was homogeneous and strong, while, obviously, changing PI from 10 to 1 cardiac cycles caused a decline of enhancement. An excellent correlation was found between DR using contrast echography and

Cutaneous vasculitis is an uncommon complication of propylthiouracil therapy. Although its pathogenesis remains to be established, detection of antineutrophil cytoplasmic antibodies (ANCA) in association with this type of vasculitis has recently been described. We report here 2 patients who developed ANCA-associated crescentic glomerulonephritis without evidence of cutaneous vasculitis during propylthiouracil treatment of hyperthyroidism. Improvement of the renal function and the disappearance of ANCA were correlately found after discontinuation of propylthiouracil and by corticosteroid therapy in both patients.

No abstract