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

Objective: Total peripheral vascular resistance (TPR) decreases in thyrotox icosis 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 plasm a 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 hor mone (TSH) 68 (38-201) mU/l, T-3 0.7 (0.35-1.5) nmol/l, fT(4) 3.0 12.0-5.9) pmol/l, median (range)) and 14 with hyperthyroidism (pretreatment: TSH 0.0 2 (<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 fr om 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 arbi trary units (AU), decreased after correction of hypothyroidism (from 1.32 < plus/minus> 0.65 to 0.96 +/- 0.36 AU, P = 0.04) and increased after correct ion of hyperthyroidism (from 0.75 +/- 0.18 to 1.10 +/- 0.35 AU, P = 0.007). Adrenomedullin concentrations did not change during the transition from th e 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 Delta fT(4) (r = -0.65, P = 0.001), log DeltaT(3), (r = -0.57, P = 0.006), Delta noradr enaline (r = 0.54, P = 0.02) and Delta ANP (atrial natriuretic peptide) (r = -0.59, P = 0.004), Multiple linear regression analysis indicated that onl y T-3 was an independent determinant of TPR. Changes in T-3 accounted for 4 6% of the variability in the changes in TPR. Conclusions: TPR is reduced in thyrotoxicosis and increased in hypothyroidi sm. Restoration of the euthyroid state normalizes TPR. Changes in TPR are n ot related to plasma adrenomedullin concentrations, but 46% could be explai ned by changes in T-3. Altered ANP secretion and adenergic tone may contrib ute to the T-3-induced changes in TPR.