title: Changes in vascular reactivity induced by acute hyperthyroidism in isolated rat aortae.
abstract: Hyperthyroidism was induced by subcutaneous injections of L-thyroxine (T(4)) (500 mg/kg/day) for 3 days in order to study whether adrenergic and muscarinic receptor-mediated vascular responses alter at an early stage of the disease. T(4) treatment was sufficient to induce a significant degree of thyroid weight loss, tachycardia, cardiac hypertrophy, and an elevation in serum T(4) levels. The tension of aortic ring preparations isolated from rats was measured isometrically to investigate the influence of acute hyperthyroidism. The contractions induced by norepinephrine (NE) were significantly suppressed in aortic rings from rats treated with T(4) compared with control rats. N(G)-nitro-L-arginine (L-NOARG), an inhibitor of nitric oxide synthase (NOS), significantly enhanced NE-induced contraction in aortic rings from both control and T(4)-treated rats, and the enhancement was greater in rats treated with T(4) than control rats. The relaxations induced by either acetylcholine (ACh) or sodium nitroprusside (SNP) were also significantly enhanced by T(4) treatment. L-NOARG abolished the relaxation induced by ACh in aortic rings from both control and T(4)-treated rats. L-NOARG shifted SNP-induced relaxation curves of aortic rings from those of control rats to the left, but not with rats treated with T(4). T(4) treatment showed no influence on the amount of endothelial NOS (eNOS) protein. These results suggest that vascular responses alter at an early stage of hyperthyroidism and that it may be due to a modification in the NO system which is independent from the amount of eNOS protein.
authors.affiliation: Department of Pharmacology, Tokyo University of Pharmacy and Life Science, 1432-1, Horinouchi, Tokyo 193-0392, Hachioji, Japan. hhonda@ps.toyaku.ac.jp
authors.forename: H
authors.initials: H
authors.lastname: Honda
authors.forename: T
authors.initials: T
authors.lastname: Iwata
authors.forename: T
authors.initials: T
authors.lastname: Mochizuki
authors.forename: H
authors.initials: H
authors.lastname: Kogo
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000208:Acute Disease; D000818:Animals; D001011:Aorta / Q000503:physiopathology*; D001794:Blood Pressure / Q000187:drug effects; D015153:Blotting, Western; D001835:Body Weight / Q000187:drug effects; D002317:Cardiovascular Agents / Q000494:pharmacology; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D006339:Heart Rate / Q000187:drug effects; D006980:Hyperthyroidism / Q000503:physiopathology*; D008297:Male; D009126:Muscle Relaxation / Q000187:drug effects; D009200:Myocardial Contraction / Q000187:drug effects; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D019001:Nitric Oxide Synthase / Q000032:analysis; D009599:Nitroprusside / Q000494:pharmacology; D009638:Norepinephrine / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D013268:Stimulation, Chemical; D013974:Thyroxine / Q000097:blood / Q000187:drug effects / Q000494:pharmacology; D014284:Triiodothyronine / Q000097:blood / Q000187:drug effects; D014661:Vasoconstriction / Q000187:drug effects / Q000502:physiology
chemical_list: D002317:Cardiovascular Agents; D014284:Triiodothyronine; D009599:Nitroprusside; D019001:Nitric Oxide Synthase; D000109:Acetylcholine; D013974:Thyroxine; D019331:NG-Nitroarginine Methyl Ester; D009638:Norepinephrine