The Direct Vasomotor Effect of Thyroid Hormones on Rat Skeletal Muscle Resistance Arteries

• Published in: Anesthesia and analgesia Vol. 85; no. 4; pp. 734 - 738
• Main Authors: Park, Kyung W, Dai, Hai B, Ojamaa, Kaie, Lowenstein, Edward, Klein, Irwin, Sellke, Frank W
• Format: Journal Article
• Language: English
• Published: Hagerstown, MD International Anesthesia Research Society 01.10.1997; Lippincott
• Subjects: 15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid; Animals; Biological and medical sciences; Endothelium, Vascular - physiology; Female; Hormones. Endocrine system; In Vitro Techniques; Male; Medical sciences; Muscle, Skeletal - blood supply; Pharmacology. Drug treatments; Prostaglandin Endoperoxides, Synthetic - pharmacology; Rats; Rats, Wistar; Thromboxane A2 - analogs & derivatives; Thromboxane A2 - pharmacology; Thyroid Hormones - pharmacology; Vascular Resistance - drug effects; Vasodilation - drug effects; Rat; Aminoacid derivative hormone; Rodentia; Striated muscle; In vitro; Artery; Vasodilation; Resistance; Vertebrata; Mammalia; Animal; Blood vessel; Thyroid hormone; Triiodothyronine; Levothyroxine sodium
• ISSN: 0003-2999; 1526-7598
• DOI: 10.1097/00000539-199710000-00005

The present study examines the hypothesis that the hormones have direct vasodilatory effects and attempts to determine whether the effects are endothelium-dependent. Rat skeletal muscle resistance arteries of approximately 100 micro m were dissected, and vessel diameter changes were monitored using a videodetection system. After equilibration at 37[degree sign]C, each vessel was preconstricted with the thromboxane analog U46619 1 micro M, and the percentage of dilation was measured after exposure to increasing concentrations of triiodothyronine (T3) or levothyroxine (T4) (10 to 10 M). Dilation in response to T3 was also measured after endothelial denudation and pretreatment with the nitric oxide (NO) synthase inhibitor N (L-NNA) 10 micro M, the cyclooxygenase inhibitor indomethacin 10 micro M, the adenosine triphosphate-sensitive K channel blocker glibenclamide 1 micro M, or the beta-adrenergic antagonist propranolol 1 micro M. Both T3 and T4 demonstrated concentration-dependent dilation of the U46619-preconstricted vessels (P < 0.001 each), with T3 having a greater effect than T4 (P < 0.05) (36% +/- 9% [mean +/- SD] dilation at 10 M T3 vs 24% +/- 6% dilation at 10 M T4). In comparison, isoproterenol 10 M produced 56% +/- 6% dilation. T3-mediated vasodilation was attenuated but not abolished by endothelial denudation (18% +/- 3% dilation at 10 M T3) (P < 0.01), L-NNA (15% +/- 7% dilation at 10 M T3) (P < 0.01), indomethacin (20% +/- 9% dilation at 10 M T3) (P < 0.05), and glibenclamide (22% +/- 7% dilation at 10 M T3) (P < 0.01), but it was not affected by propranolol (37% +/- 20% dilation at 10 M T3) (P = 0.99). We conclude that thyroid hormones possess direct vasodilatory effects with both endothelium-independent and endothelium-dependent components. ImplicationsThyroid hormones may have modest direct vasodilatory effects. This may partially account for the cardiovascular actions of the hormones in hyperthyroidism or when administered pharmacologically in cardiac surgery.(Anesth Analg 1997;85:734-8)