title: Decrease in renal medullary endothelial nitric oxide synthase of fructose-fed, salt-sensitive hypertensive rats.
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. kg(-1). day(-1)), 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, 129+/-4 mm Hg, versus LS-F rats, 115+/-3 mm Hg, P<0.05; or versus HS-C rats, 116+/-5 mm Hg, P<0.05), 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, 129+/-4 mm Hg, versus HS-FP rats, 113+/-3 mm Hg, P<0.05) 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.
authors.affiliation: Internal Medicine II, Nagoya University School of Medicine, Nagoya, Japan. nisimoto@med.nagoya-u.ac.jp
authors.forename: Yasuhiro
authors.initials: Y
authors.lastname: Nishimoto
authors.forename: Takahito
authors.initials: T
authors.lastname: Tomida
authors.forename: Hideo
authors.initials: H
authors.lastname: Matsui
authors.forename: Takayuki
authors.initials: T
authors.lastname: Ito
authors.forename: Kenji
authors.initials: K
authors.lastname: Okumura
mesh_terms: D000818:Animals; D001011:Aorta / Q000187:drug effects / Q000201:enzymology; D001794:Blood Pressure / Q000187:drug effects; D019422:Dietary Sucrose / Q000008:administration & dosage; D005632:Fructose / Q000008:administration & dosage*; D006973:Hypertension / Q000503:physiopathology*; D007004:Hypoglycemic Agents / Q000494:pharmacology; D007672:Kidney Cortex / Q000187:drug effects / Q000378:metabolism; D007679:Kidney Medulla / Q000187:drug effects* / Q000201:enzymology; D008297:Male; D019001:Nitric Oxide Synthase / Q000378:metabolism*; D052250:Nitric Oxide Synthase Type III; D000077205:Pioglitazone; D012333:RNA, Messenger / Q000187:drug effects / Q000235:genetics / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D017673:Sodium Chloride, Dietary / Q000008:administration & dosage*; D013844:Thiazoles / Q000494:pharmacology; D045162:Thiazolidinediones; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics
chemical_list: D019422:Dietary Sucrose; D007004:Hypoglycemic Agents; D012333:RNA, Messenger; D017673:Sodium Chloride, Dietary; D013844:Thiazoles; D045162:Thiazolidinediones; D014409:Tumor Necrosis Factor-alpha; D005632:Fructose; D019001:Nitric Oxide Synthase; D052250:Nitric Oxide Synthase Type III; C496316:Nos3 protein, rat; D000077205:Pioglitazone