Ladenson P W, Langevin H, Michener M
Division of Endocrinology and Metabolism, Sinai Hospital of Baltimore, Maryland 21215.
J Clin Endocrinol Metab. 1987 Dec;65(6):1172-6. doi: 10.1210/jcem-65-6-1172.
Atriopeptin (AP) is a polypeptide produced by atrial myocytes that is capable of inducing diuresis, natriuresis, and vasodilatation. Because thyroid dysfunction is known to be associated with alterations in both renal function and vasomotor control, we investigate the possible effects of varying thyroid function on AP in humans and rats. Plasma AP concentrations were determined in hyperthyroid and hypothyroid patients and normal subjects. Plasma AP was also measured in some patients after the iv infusion of 1 L 150 mmol/L NaCl and after treatment of hyperthyroidism or hypothyroidism. Plasma and atrial AP concentrations were measured in hyperthyroid, euthyroid, and hypothyroid rats. Plasma AP concentrations did not differ in the hyperthyroid (n = 22), euthyroid (n = 45), and hypothyroid (n = 16) subjects [47.1 +/- 18.2 (mean +/- SD), 45.1 +/- 28.9, and 42.4 +/- 20.0 pg/mL, respectively]. After NaCl infusion, mean plasma AP concentrations did not increase significantly in any of the three groups. Treatment of hyperthyroidism and hypothyroidism did not result in a significant change in plasma AP levels. In contrast, plasma AP concentrations were significantly higher in T4-treated (hyperthyroid) rats than in either euthyroid or propylthiouracil-treated (hypothyroid) rats [621 +/- 17 vs. 266 +/- 41 (P less than 0.01) and 210 +/- 28 pg/mL (P less than 0.001), respectively], whereas atrial AP contents were similar in the three groups of rats. We conclude that hyperthyroidism and hypothyroidism in man are not associated with significantly altered plasma AP concentrations. The higher plasma AP levels in T4-treated rats may reflect the relatively shorter duration or greater severity of thyroid dysfunction or thyroid hormone-induced myocardial hypertrophy in the animals.
心钠素（AP）是一种由心房肌细胞产生的多肽，能够诱导利尿、利钠和血管舒张。由于已知甲状腺功能障碍与肾功能和血管舒缩控制的改变有关，我们研究了甲状腺功能变化对人和大鼠体内AP的可能影响。测定了甲状腺功能亢进和减退患者以及正常受试者的血浆AP浓度。还在一些患者静脉输注1L 150mmol/L氯化钠后以及治疗甲状腺功能亢进或减退后测量了血浆AP。测定了甲状腺功能亢进、甲状腺功能正常和甲状腺功能减退大鼠的血浆和心房AP浓度。甲状腺功能亢进组（n = 22）、甲状腺功能正常组（n = 45）和甲状腺功能减退组（n = 16）受试者的血浆AP浓度无差异[分别为47.1±18.2（平均值±标准差）、45.1±28.9和42.4±20.0 pg/mL]。输注氯化钠后，三组中任何一组的平均血浆AP浓度均未显著升高。治疗甲状腺功能亢进和减退并未导致血浆AP水平发生显著变化。相比之下，T4治疗（甲状腺功能亢进）大鼠的血浆AP浓度显著高于甲状腺功能正常或丙硫氧嘧啶治疗（甲状腺功能减退）大鼠[分别为621±17与266±41（P＜0.01）和210±28 pg/mL（P＜0.001）]，而三组大鼠的心房AP含量相似。我们得出结论：人类甲状腺功能亢进和减退与血浆AP浓度的显著改变无关。T4治疗大鼠血浆AP水平较高可能反映了动物甲状腺功能障碍的持续时间相对较短或严重程度较高，或者是甲状腺激素诱导的心肌肥大。
