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The Journal of Clinical Endocrinology & Metabolism Vol. 89, No. 7 3455-3461
Copyright © 2004 by The Endocrine Society

Thyroid Function and Blood Pressure Homeostasis in Euthyroid Subjects

Olga Gumieniak, Todd S. Perlstein, Paul N. Hopkins, Nancy J. Brown, Laine J. Murphey, Xavier Jeunemaitre, Norman K. Hollenberg and Gordon H. Williams

Endocrinology, Diabetes and Hypertension Division, Department of Medicine (O.G., T.S.P., G.H.W.), and Department of Radiology (N.K.H.), Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts 02115; Department of Cardiovascular Genetics, Cardiology Division (P.N.H.), University of Utah, Salt Lake City, Utah 84112; Department of Medicine (N.J.B., L.J.M.), Vanderbilt University, Nashville, Tennessee 37232; and Department of Genetics and Clinical Investigation Centre (X.J.), Hôpital Europeen Georges Pompidou, Paris 75908, France

Address all correspondence and requests for reprints to: Gordon H. Williams, M.D., Endocrine-Hypertension Division, 221 Longwood Avenue, RFB-2, Boston, Massachusetts 02115. E-mail: gwilliams{at}partners.org.

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 T4 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 (ß = –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 (ß = –1.42, P = 0.008) and hypertensive subjects (ß = –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.

This research was supported by the following grants: National Institutes of Health (NIH) Grants HL47651, HL59424, and DK63214; Specialized Center of Research in Hypertension from the National Heart, Lung and Blood Institute Grant HL55000; National Center for Research Resources (General Clinical Research Centers), Boston, Massachusetts (M01 RR 02635), Salt Lake City, Utah (M01 RR 00064), and Vanderbilt, Nashville, Tennessee (M01 RR 00095). O.G. and T.S.P. were supported in part by the NIH Training Grant T32 HL007609.

Abbreviations: BMI, Body mass index; CI, confidence interval; DBP, diastolic blood pressure; ERPF, effective renal plasma flow; FTI, free T4 index; HOMA, homeostasis model assessment; MAP, mean arterial pressure; OR, odds ratio; PRA, plasma renin activity; RVR, renal vascular resistance; THBR, thyroid hormone binding ratio.




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