Thyroid hormones and vascular reactivity: role of the endothelial cell.
Decreased maximal responses to noradrenaline, adrenaline and phenylephrine were observed in aortas isolated from rats pretreated with triiodothyronine and thyroxine for 8 days. In addition, a potent relaxant effect occurred when supramaximal concentrations of noradrenaline and adrenaline, but not of phenylephrine, were used. The relaxant effect was not observed in preparations in which the endothelium had been removed, and it was antagonized by propranolol added to the bathing fluid. Practolol was ineffective. In vivo, adrenaline and noradrenaline evoked pressor effects which were of shorter duration and smaller magnitude in hormone-treated animals than in the controls. Furthermore, a subsequent fall in blood pressure to below normal was observed, not only with adrenaline but also with noradrenaline, in animals receiving thyroid hormones. We conclude that when large amounts of thyroid hormones circulate in the body, large arteries are more prone to distention in the presence of increased quantities of released catecholamines, and resistance vessels are less responsive to their pressor effects due to a superimposing dilator effect. These changes might represent adaptative mechanisms in hyperthyroid states, and might depend on a greater sensitivity of endothelial beta 2-receptors to noradrenaline and adrenaline.
D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D004727:Endothelium / Q000187:drug effects* / Q000502:physiology; D066298:In Vitro Techniques; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains; D013566:Sympathomimetics / Q000494:pharmacology*; D013963:Thyroid Hormones / Q000494:pharmacology*; D013974:Thyroxine / Q000494:pharmacology; D014284:Triiodothyronine / Q000494:pharmacology; D014661:Vasoconstriction / Q000187:drug effects
D013566:Sympathomimetics; D013963:Thyroid Hormones; D014284:Triiodothyronine; D013974:Thyroxine