Endocrine factors related to changes in total peripheral vascular resistance after treatment of thyrotoxic and hypothyroid patients

Abstract

Objective: Total peripheral vascular resistance (TPR) decreases in thyrotoxicosis and increases in hypothyroidism. Several mechanisms may be involved, including adaptation to changes in heat production and direct non-genomic effects of tri-iodothyronine (T 3 ) on vascular smooth muscle cells. The aim of this study was to see if changes in TPR are related to changes in plasma concentrations of the endothelial hormones adrenomedullin and endothelin-1 as well as other hormones affecting vasculature. Design: A prospective study. Subjects: Eleven hypothyroid patients (pretreatment: thyroid-stimulating hormone (TSH) 68 (38±201) mU/l, T 3 0.7 (0.35±1.5) nmol/l, fT 4 3.0 (2.0±5.9) pmol/l, median (range)) and 14 with hyperthyroidism (pretreatment: TSH 0.02 (,0.01±0.06) mU/l, T 3 6.4 (2.3±13.0) nmol/l, fT 4 56.1 (22.9±70.0) pmol/l) were studied before treatment and 3 months after reaching the euthyroid state. Blood collection was carried out simultaneously with the recording of finger arterial pressure (FINAP). Cardiac output and TPR were derived from stroke volume computations by modelling flow from the FINAP signal. Results: Thyroid-function tests of hypothyroid and thyrotoxic patients did not differ after restoration of the euthyroid state. TPR, expressed in arbitrary units (AU), decreased after correction of hypothyroidism (from 1X32^0X65 to 0X96^0X36 AU, P 0X04 and increased after correction of hyperthyroidism (from 0X75^0X18 to 1X10^0X35 AU, P 0X007X Adrenomedullin concentrations did not change during the transition from the hypothyroid state 3.2(0.9±11.0) pmol/l to the euthyroid state 4.9(0.9±8.6) pmol/l, but decreased after treatment of hyperthyroidism, from 5.2(0.9±11.0) pmol/l to 2.2(0.9±5.4) pmol/l. Plasma endothelin-1 was undetectable in all samples. Changes in TPR upon treatment correlated with log DfT 4 r 20X65Y P 0X001Y log DT 3 Y r 20X57Y P 0X006Y D noradrenaline r 0X54Y P 0X02 and D ANP (atrial natriuretic peptide) r 20X59Y P 0X004X Multiple linear regression analysis indicated that only T 3 was an independent determinant of TPR. Changes in T 3 accounted for 46% of the variability in the changes in TPR. Conclusions: TPR is reduced in thyrotoxicosis and increased in hypothyroidism. Restoration of the euthyroid state normalizes TPR. Changes in TPR are not related to plasma adrenomedullin concentrations, but 46% could be explained by changes in T 3 . Altered ANP secretion and adenergic tone may contribute to the T 3 -induced changes in TPR.

Folic Acid Alleviates Oxidative Stress and Hyperhomocysteinemia Involved in Liver Dysfunction of Hypothyroid Rats

“…In the present study serum Hcy in hypothyroid rats were significantly higher than those found in the control, also Hcy in hypothyroid rats which treated with folic acid during and after inducing hypothyroidism were insignificantly lower than those found in the hypothyroid rats. This finding is in line with that of Diekman et al [35] nd Ibrahim et al [4] who reported that plasma Hcy concentrations increased in hypothyroidism and decreased in hyperthyroidism the mechanism of thyroid-induced changes in homocysteine metabolism is currently unknown. Adrees et al [36] who observed that total Hcy levels were elevated in patients with subclinical and overt hypothyroidism.…”

Thyroid Disease and the Heart

“…29 Adrenomedullin, a polypeptide of 52 amino acids, is a potent vasodilator transcriptionally regulated by thyroid hormone, and serum levels are increased in thyrotoxicosis. 33 Interestingly, however, Diekman and colleagues 34 demonstrated that although SVR is decreased and adrenomedullin is increased in thyrotoxicosis, restoration of euthyroidism normalized SVR but was not correlated with plasma adrenomedullin levels. In the present study, only T 3 was an independent determinant of SVR.…”

Effect of Thyroxine Replacement on Creatinine, Insulin-Like Growth Factor 1, Acid-Labile Subunit, and Vascular Endothelial Growth Factor

“…A decrease in peripheral vascular resistance and in diastolic blood pressure may also be related to enhanced NO production and has been Clinical Chemistry 50, No. 1,2004 found in hypothyroid patients treated with thyroxine (23)(24)(25).…”