Quesada Andrés, Sainz Juan, Wangensteen Rosemary, Rodriguez-Gomez Isabel, Vargas Félix, Osuna Antonio
Departamento de Fisiología de la Facultad de Medicina de Granada, Granada, Spain.
Eur J Endocrinol. 2002 Jul;147(1):117-22. doi: 10.1530/eje.0.1470117.
Thyroid disorders are accompanied by important changes in haemodynamic and cardiac functions and renal sodium handling. Since nitric oxide (NO) plays a crucial role in regulating vascular tone and renal sodium excretion, the present paper was designed to determine whether changes in the activity of NO synthase (NOS) participate in the cardiovascular and renal manifestations of thyroid disorders.
We measured NOS activity in the heart (left and right ventricles), vessels (aorta and cava) and kidney (cortex and medulla) of euthyroid, hyperthyroid and hypothyroid rats after 6 weeks of treatment. NOS activity was determined by measuring the conversion of L-[(3)H]-arginine to L-[(3)H]-citruline.
NOS activity was higher in all tissues from hyperthyroid rats when compared with controls, except in the right ventricle. In the hypothyroid group, NOS activity showed a more heterogeneous pattern, with significant increases in both ventricles but significant reduction in the aorta, while in the vena cava, renal cortex and medulla the enzyme activity also tended to be higher, but significance was not reached.
These data indicated that NOS activity was upregulated in tissues primarily related to blood pressure control in hyperthyroid rats, suggesting that an increased NO production may contribute to the hyperdynamic circulation in hyperthyroidism and may have a protective homeostatic effect in the target organs of the hypertension that accompanies this endocrine disease. The aortic and renal findings in hypothyroid rats suggested a possible role for NOS in the increased peripheral resistance and the normal pressure-diuresis-natriuresis response of these hypotensive animals, although hypothyroidism produced a heterogeneous tissue response in NOS activity.
甲状腺疾病伴有血流动力学、心脏功能及肾脏钠代谢的重要改变。由于一氧化氮（NO）在调节血管张力和肾脏钠排泄中起关键作用，本文旨在确定一氧化氮合酶（NOS）活性的变化是否参与甲状腺疾病的心血管及肾脏表现。
我们测定了经过6周治疗的甲状腺功能正常、甲状腺功能亢进及甲状腺功能减退大鼠的心脏（左心室和右心室）、血管（主动脉和腔静脉）及肾脏（皮质和髓质）中的NOS活性。通过测量L-[(3)H]-精氨酸向L-[(3)H]-瓜氨酸的转化来确定NOS活性。
与对照组相比，甲状腺功能亢进大鼠所有组织中的NOS活性均较高，但右心室除外。在甲状腺功能减退组中，NOS活性呈现出更为异质性的模式，两个心室中的活性显著增加，而主动脉中的活性显著降低，同时在腔静脉、肾皮质和髓质中，该酶活性也有升高趋势，但未达到显著水平。
这些数据表明，甲状腺功能亢进大鼠中主要与血压控制相关的组织中的NOS活性上调，提示NO生成增加可能有助于甲状腺功能亢进时的高动力循环，并且可能对伴随这种内分泌疾病的高血压的靶器官具有保护性稳态作用。甲状腺功能减退大鼠的主动脉和肾脏研究结果表明，NOS可能在这些低血压动物的外周阻力增加及正常压力-利尿-利钠反应中发挥作用，尽管甲状腺功能减退在NOS活性方面产生了异质性的组织反应。
