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Nitric oxide mediates abnormal responsiveness of thyroid arteries in methimazole-treated patients

¹ Department of Surgery, ² Hospital Clínico Research Unit and ³ Department of Physiology, University of Valencia, 46010 Valencia, Spain

(Correspondence should be addressed to S Lluch, Departamento de Fisiología, Facultad de Medicina, Blasco Ibañez 17, 46010 Valencia, Spain; Email: lluchs{at}post.uv.es)

Objective: We studied the intervention of nitric oxide (NO), prostacyclin and endothelium-derived hyperpolarizing factor (EDHF) in mediating responses to acetylcholine in thyroid arteries from euthyroid and methimazole-treated (MT) patients.

Design and methods: Branches of the superior thyroid artery were obtained from 19 euthyroid patients and 17 MT patients (euthyroid at the time of surgery) undergoing total thyroidectomy or hemithyroidectomy. Artery rings were suspended in organ baths for isometric recording of tension.

Results and conclusions: Acetylcholine caused endothelium-dependent relaxation of greater magnitude in arteries from MT patients (pD₂ (–log EC₅₀) values were 7.68±0.19 in euthyroid and 8.17±0.26 in MT patients, P <0.05). The relaxation was unaffected by indomethacin and was partially reduced by the NO-synthase inhibitor NG-monomethyl-L-arginine (L-NMMA). This reduction was higher in arteries from MT patients (50±6%) as compared with euthyroid patients (36±6%) (P <0.05). Inhibition of K⁺ channels using apamin combined with charybdotoxin or high K⁺ solution abolished the relaxation resistance to L-NMMA and indomethacin. The maximal contraction response to noradrenaline (as a percentage of the response to 100 mM KCl) was lower in MT than in euthyroid patients (57±10 and 96±8 respectively, P < 0.05). The hyporesponsiveness to noradrenaline in arteries from MT patients was corrected by L-NMMA. The results indicate that: (i) thyroid arteries from MT patients show an increased relaxation response to acethylcholine and a decreased contraction response to noradrenaline due to overproduction of NO; (ii) EDHF plays a prominent role in acetylcholine-induced relaxation through activation of Ca²⁺-activated K⁺ channels; (iii) the abnormal endothelium-dependent responses in arteries from MT patients are not corrected by medical treatment.