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

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

dc.contributor.author	Ortega Serrano, Joaquín
dc.contributor.author	Vila Salinas, José María
dc.contributor.author	Mauricio Aviñó, María Dolores
dc.contributor.author	Segarra Irles, Gloria Vicenta
dc.contributor.author	Medina Bessó, Pascual
dc.contributor.author	Martínez León, Juan Bautista
dc.contributor.author	Lluch, Salvador
dc.date.accessioned	2013-11-21T09:48:54Z
dc.date.available	2013-11-21T09:48:54Z
dc.date.issued	2005
dc.identifier.citation	Ortega Serrano, Joaquín Vila, José María Mauricio Aviñó, María Dolores Segarra, Gloria Medina, Pascual Martínez León, Juan Bautista Lluch, Salvador 2005 Nitric oxide mediates abnormal responsiveness of thyroid arteries in methimazole-treated patients European Journal of Endocrinology 152 4 551 556
dc.identifier.uri	http://hdl.handle.net/10550/31185
dc.description.abstract	Objective: We studied the intervention of nitric oxide (NO), prostacyclin (PGI2) and endothelium-derived hyperpolarizing factor (EDHF) in mediating responses to acetylcholine in thyroid arteries from euthyroid (E) and methimazole-treated (MT) patients. Design and methods: Branches of the superior thyroid artery were obtained from 19 E 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 7.68±0.19 in E and 8.17±0.26 in MT, P<0.05). The relaxation was unaffected by indomethacin and partially reduced by the NO synthase inhibitor L-NMMA. This reduction was higher in arteries from MT patients (50±6 %) as compared to E patients (36±6 %) (P<0.05). Inhibition of K+ channels using apamin combined with charybdotoxin or high K+ solution abolished the relaxation resistant to L-NMMA and indomethacin. The maximal contractions to noradrenaline (in percentage of the response to 100 mM KCl) were lower in MT than in E 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: (1) thyroid arteries from MT patients show increased relaxation to acethylcholine and decreased contraction to noradrenaline due to overproduction of NO; (2) EDHF plays a prominent role in acetylcholine-induced relaxation through activation of Ca2+-activated K+ channels; (3) the abnormal endothelium-dependent responses in arteries from MT patients are not corrected by medical treatment.
dc.relation.ispartof	European Journal of Endocrinology, 2005, vol. 152, num. 4, p. 551-556
dc.subject	Tiroide Malalties
dc.subject	Òxid nítric
dc.title	Nitric oxide mediates abnormal responsiveness of thyroid arteries in methimazole-treated patients
dc.type	journal article	es_ES
dc.date.updated	2013-11-21T09:48:54Z
dc.identifier.idgrec	016614
dc.rights.accessRights	open access	es_ES