Abstract-We investigated the expression of endothelial NO synthase (eNOS) in the kidneys of fructose-fed insulin-resistant rats (FFR) with a low-or high-sodium diet. Male Sprague-Dawley rats were fed a control (C) or high-fructose (40% fructose; F) diet, with each coming in low-sodium (0.024% NaCl; LS-C or LS-F) or high-sodium (3% NaCl; HS-C or HS-F) varieties, for 2 weeks. Half of the FFR were orally administered pioglitazone (10 mg ⅐ kg Ϫ1 ⅐ day Ϫ1 ), an insulin-sensitizing agent (LS-FP or HS-FP). The systolic blood pressure was significantly higher in the HS-F rats than in the LS-F rats or the HS-C rats (HS-F rats, 129Ϯ4 mm Hg, versus LS-F rats, 115Ϯ3 mm Hg, PϽ0.05; or versus HS-C rats, 116Ϯ5 mm Hg, PϽ0.05), which indicated the salt dependence of hypertension in FFR. The protein expression of eNOS in the renal medulla of FFR was significantly lower than that in control rats during a high sodium load. The administration of pioglitazone prevented the hypertension (HS-F rats, 129Ϯ4 mm Hg, versus HS-FP rats, 113Ϯ3 mm Hg, PϽ0.05) and the reduction of medullary eNOS protein expression in HS-F rats. There was no significant difference in eNOS expression in the renal cortex or aorta between FFR and control rats, regardless of sodium load. These results suggest that the decrease in renal medullary NO production by eNOS during a high sodium load may play a role in fructose-fed, salt-sensitive hypertension. Key Words: insulin resistance Ⅲ fructose Ⅲ hypertension, sodium-dependent Ⅲ nitric oxide synthase Ⅲ kidney P revious studies have shown an association between insulin resistance and systemic hypertension. 1,2 Compensatory hyperinsulinemia was thought to cause hypertension because it led to sodium retention, sympathetic nerve activation, and vascular smooth muscle cell proliferation. 2 However, Bursztyn et al 3 demonstrated that chronic exogenous hyperinsulinemia itself did not elevate blood pressure; only when in combination with a defective NO system, might hyperinsulinemia cause hypertension. Some investigators revealed a correlation between insulin resistance and defects of the NO system, 4,5 and others have shown that a defective NO system in the kidney 6 or the whole body 7 could be the cause of hypertension.Renal NO is an important controller of urinary sodium excretion, 8 so a defect of the NO system in the kidney can become the cause of salt-sensitive hypertension. 6,9,10 If the defect of the NO system is seen in the kidney of insulin-resistant subjects, they may develop salt-sensitive hypertension. Indeed, several investigators indicate that patients 11,12 or animals 13,14 with insulin resistance tend to develop saltsensitive hypertension. Although the mechanisms underlying the coexistence of insulin resistance and hypertension remain unclear, a defect of the NO system in the kidney is thought to be a cause of hypertension in insulin-resistant subjects. 13 NO is produced from the conversion of L-arginine to L-citrulline by a family of enzymes known as NO synthase (NOS). 15 NOS exists in 3 isoforms: neuronal ...

These data indicate that an increase in COX-2 expression might have a hypertensive effect, partly associated with 8-iso-PGF(2alpha) formation in l-NAME-treated rats.

A 72-year-old womanwas admitted for recurrent episodes of encephalopathy. Laboratory data showedmild liver dysfunction and hyperammonemia, while she had neither anemia nor splenomegaly. The dilated inferior mesenteric vein (IMV) was opacified retrogradely from the superior mesenteric vein by superior mesenteric arteriography, and IMVwas found to connect with the inferior vena cava (IVC) through a torturous shunt. Noobstruction of the extrahepatic portal vein or hepatic vein was observed by arteriography. Histological evaluation of the liver biopsy indicated remarkable fatty change without cirrhosis. Finally, we diagnosed this case as extrahepatic portosystemic venous shunt without portal hypertension.

Enhanced secretion of insulin during the OGTT might be useful as a predictor of coronary atherosclerosis and of restenosis after elective PTCA in nondiabetic patients with effort angina.

This newly proposed method could be a simple and practical way to automatically reduce misregistration artifacts in DSA.