Gumieniak Olga, Perlstein Todd S, Hopkins Paul N, Brown Nancy J, Murphey Laine J, Jeunemaitre Xavier, Hollenberg Norman K, Williams Gordon H
Endocrinology, Diabetes and Hypertension Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, 221 Longwood Avenue, RFB-2, Boston, MA 02115, USA.
J Clin Endocrinol Metab. 2004 Jul;89(7):3455-61. doi: 10.1210/jc.2003-032143.
Overt and subclinical hypothyroidism are associated with increased systemic vascular resistance and hypertension. We examined the relationship between thyroid function and blood pressure homeostasis in euthyroid individuals. A total of 284 subjects (68% hypertensive) consumed high- (200 mmol) and low- (10 mmol) sodium diets, and their blood pressure responses were assessed as percentage change in the mean arterial pressure (MAP). p-Aminohippuric acid clearance was used to estimate effective renal plasma flow. Renal vascular resistance (RVR) was calculated as MAP divided by effective renal plasma flow. Serum free T(4) index (FTI) was lower (P < 0.0001) and TSH was higher (P = 0.046) in hypertensive compared with normotensive subjects independent of other baseline characteristics. FTI (beta = -1.51, P < 0.0001), baseline MAP, and race independently predicted MAP salt sensitivity. The FTI relationship with salt sensitivity adjusted for baseline MAP and race was similar among normotensive (beta = -1.42, P = 0.008) and hypertensive subjects (beta = -1.66, P = 0.0001). FTI correlated negatively with high- (P = 0.0001) and low- (P = 0.008) salt RVR, whereas TSH correlated positively with high- (P = 0.016) and low- (P = 0.012) salt RVR independent of age, gender, race, and body mass index. We have found that FTI is lower and TSH is higher in hypertensive compared with normotensive euthyroid subjects and that FTI independently predicts blood pressure salt sensitivity. These data show that the influence of thyroid function on blood pressure homeostasis extends into euthyroid range and likely reflects the action of thyroid hormone on peripheral vasculature.
显性和亚临床甲状腺功能减退与全身血管阻力增加和高血压有关。我们研究了甲状腺功能正常个体的甲状腺功能与血压稳态之间的关系。共有284名受试者(68%为高血压患者)食用高钠(200 mmol)和低钠(10 mmol)饮食,并将其血压反应评估为平均动脉压(MAP)的变化百分比。对氨基马尿酸清除率用于估计有效肾血浆流量。肾血管阻力(RVR)计算为MAP除以有效肾血浆流量。与血压正常的受试者相比,高血压受试者的血清游离T4指数(FTI)较低(P<0.0001),促甲状腺激素(TSH)较高(P=0.046),且不受其他基线特征影响。FTI(β=-1.51,P<0.0001)、基线MAP和种族可独立预测MAP盐敏感性。在血压正常(β=-1.42,P=0.008)和高血压受试者(β=-1.66,P=0.0001)中,调整基线MAP和种族后,FTI与盐敏感性的关系相似。FTI与高盐(P=0.0001)和低盐(P=0.008)RVR呈负相关,而TSH与高盐(P=0.016)和低盐(P=0.012)RVR呈正相关,且不受年龄、性别、种族和体重指数影响。我们发现,与血压正常的甲状腺功能正常受试者相比,高血压受试者的FTI较低,TSH较高,且FTI可独立预测血压盐敏感性。这些数据表明,甲状腺功能对血压稳态的影响延伸至甲状腺功能正常范围,可能反映了甲状腺激素对外周血管系统的作用。