Departamento de Fisiología, Universidad de Valencia, 46010 Valencia, Spain; Instituto de Investigación Sanitaria INCLIVA, Hospital Clínico Universitario, 46010 Valencia, Spain.
Life Sci. 2013 Oct 10;93(15):525-9. doi: 10.1016/j.lfs.2013.08.019. Epub 2013 Aug 31.
In the present study we investigated the intervention of nitric oxide and prostacyclin in the responses to vasopressin of isolated thyroid arteries obtained from multi-organ donors.
Paired artery rings from glandular branches of the superior thyroid artery, one normal and the other deendothelised, were mounted in organ baths for isometric recording of tension. Concentration-response curves to vasopressin were determined in the absence and in the presence of either the vasopressin V1 receptor antagonist d(CH2)5Tyr(Me)AVP (10(-8)M), the nitric oxide synthase inhibitor N(G)-monomethyl-l-arginine (L-NMMA, 10(-4)M), or the inhibitor of prostaglandins indomethacin (10(-6)M).
In artery rings under resting tension, vasopressin produced concentration-dependent, endothelium-independent contractions. The vasopressin V1 receptor antagonist d(CH2)5Tyr(Me)AVP (10(-8)M) displaced the control curve to vasopressin 19-fold to the right in a parallel manner. The contractile response to vasopressin was unaffected by L-NMMA or by indomethacin.
Vasopressin causes constriction of human thyroid arteries by stimulation of V1 vasopressin receptors located on smooth muscle cells. These effects are not linked to the presence of an intact endothelium or to the release of nitric oxide or prostaglandins. The constriction of thyroid arteries may be particularly relevant in certain pathophysiological circumstances in which vasopressin is released in amounts that could interfere with the blood supply to the thyroid gland.
本研究旨在探讨一氧化氮和前列环素对从多器官供体获得的甲状腺动脉对血管加压素反应的干预作用。
将来自甲状腺上动脉腺支的成对动脉环（一个正常，另一个去内皮化）安装在器官浴中，用于等长张力记录。在没有和存在血管加压素 V1 受体拮抗剂 d(CH2)5Tyr(Me)AVP（10(-8)M）、一氧化氮合酶抑制剂 N(G)-单甲基-l-精氨酸 (L-NMMA，10(-4)M）或前列腺素抑制剂吲哚美辛（10(-6)M）的情况下，确定血管加压素的浓度-反应曲线。
在静息张力下的动脉环中，血管加压素产生浓度依赖性、内皮非依赖性收缩。血管加压素 V1 受体拮抗剂 d(CH2)5Tyr(Me)AVP（10(-8)M）以平行方式将对照曲线向右移位 19 倍，得到血管加压素的 19 倍。血管加压素的收缩反应不受 L-NMMA 或吲哚美辛的影响。
血管加压素通过刺激位于平滑肌细胞上的 V1 血管加压素受体引起人甲状腺动脉收缩。这些作用与完整的内皮细胞或一氧化氮或前列腺素的释放无关。甲状腺动脉的收缩在某些病理生理情况下可能特别相关，其中血管加压素以可能干扰甲状腺血流供应的量释放。
