title: Acute hyperthyroidism alters adrenoceptor- and muscarinic receptor-mediated responses in isolated rat renal and femoral arteries.
abstract: The effects of acute hyperthyroidism on the vasorelaxing responses to isoprenaline and acetylcholine were investigated in isolated rat renal and femoral arteries. In the renal artery, isoprenaline- and acetylcholine-induced relaxations were significantly greater in hyperthyroid rats than in control rats. In the femoral artery, only the acetylcholine-induced relaxation was significantly greater in hyperthyroid rats than in control rats. In the renal artery, NG-nitro-L-arginine (L-NOARG), an inhibitor of nitric oxide (NO) synthase, reduced isoprenaline- and acetylcholine-induced relaxations in both hyperthyroid and control rats and the isoprenaline-induced relaxation was still greater in hyperthyroid rats than in control rats, but no difference in the acetylcholine-induced relaxation was seen between the two groups of rats since L-NOARG almost abolished the acetylcholine-induced relaxation. In the femoral artery, L-NOAGR reduced the isoprenaline-induced relaxation in control rats but not in hyperthyroid rats, while it almost abolished the acetylcholine-induced relaxation in both groups of rats. 17-Octadecynoic acid (17-ODYA), a cytochrome P-450 monooxygenase inhibitor, reduced the isoprenaline-induced relaxation in renal and femoral arteries from hyperthyroid and control rats, but it did not change the acetylcholine-induced relaxation in both arteries. These results indicate that acute hyperthyroidism significantly enhances beta-adrenoceptor-mediated relaxation of the renal artery and muscarinic receptor-mediated relaxation of both renal and femoral arteries, suggesting that these effects may be due to an alteration in the NO and cytochrome P-450 systems of the artery.
authors.affiliation: Second Department of Physiology, School of Medicine, Showa University, Hatanodai 1-5-8, Shinagawa, Tokyo, 142-8555, Japan.
authors.forename: Takeshi
authors.initials: T
authors.lastname: Iwata
authors.forename: Hideo
authors.initials: H
authors.lastname: Honda
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000208:Acute Disease; D000818:Animals; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology; D005231:Fatty Acids, Unsaturated / Q000494:pharmacology; D005263:Femoral Artery / Q000187:drug effects / Q000473:pathology / Q000502:physiology*; D006339:Heart Rate / Q000187:drug effects; D006980:Hyperthyroidism / Q000139:chemically induced* / Q000503:physiopathology; D007213:Indomethacin / Q000494:pharmacology; D007545:Isoproterenol / Q000037:antagonists & inhibitors / Q000494:pharmacology; D007564:Japan; D008297:Male; D009131:Muscle, Smooth, Vascular; D019335:Nitroarginine / Q000494:pharmacology; D009599:Nitroprusside / Q000494:pharmacology; D009929:Organ Size / Q000187:drug effects; D051381:Rats; D017208:Rats, Wistar; D011941:Receptors, Adrenergic / Q000502:physiology*; D011976:Receptors, Muscarinic / Q000502:physiology*; D012077:Renal Artery / Q000187:drug effects / Q000473:pathology / Q000502:physiology*; D013974:Thyroxine / Q000008:administration & dosage / Q000009:adverse effects / Q000097:blood; D014664:Vasodilation / Q000187:drug effects
chemical_list: D016861:Cyclooxygenase Inhibitors; D005231:Fatty Acids, Unsaturated; D011941:Receptors, Adrenergic; D011976:Receptors, Muscarinic; D009599:Nitroprusside; D019335:Nitroarginine; C047008:17-octadecynoic acid; D007545:Isoproterenol; D000109:Acetylcholine; D013974:Thyroxine; D007213:Indomethacin