ALPHA(2)-ADRENERGIC ACTIVITY IS NORMAL IN PATIENTS WITH THYROID-DISEASE

OBJECTIVE Several studies indicate an inverse relationship between the sympathetic nervous system activity and thyroid function. Altered adr enoceptor sensitivity, particularly alpha(1) and beta, have been descr ibed in hypothyroid and hyperthyroid patients. No information in patie nts with thyroid disease is available on the main mechanism regulating sympathetic nervous system outflow, i.e. the alpha(2)-adrenoceptor pa thway. In our study we evaluated alpha(2)-adrenergic activity in patie nts with thyroid disease by the assessment of cardiovascular and catec holamine response to clonidine, a central alpha(2) adrenergic agonist. PATIENTS Ten patients with hypothyroidism, six patients with hyperthy roidism before and during adequate therapy, and ten healthy subjects. MEASUREMENTS After three blood samples for the basal determination of noradrenaline and adrenaline, the subjects swallowed 4 mu g/kg body we ight of clonidine. Blood pressure and pulse rate were measured 30, 60, 90, 120, 130 and 140 minutes after clonidine administration; blood sa mples for determination of catecholamines were drawn at 120, 130 and 1 40 minutes. RESULTS At presentation the decrease in plasma noradrenali ne after clonidine in the patients was similar to that of the control group (hypothyroids: 1.07+/-0.23 nmol/l mean +/- SEM; hyperthyroids: 0 .54+/-0.06 nmol/l; controls: 0.36+/-0.10 nmol/l; F=1.2, P=NS). No diff erences were detected in the fall in adrenaline and mean arterial pres sure (MAP) after clonidine. The adequate therapy induced in hypothyroi d patients a decrease in the basal levers of noradrenaline (1.88+/-0.2 8 vs 0.67+/-0.10 nmol/l; P<005) and a lesser fair in mean arterial pre ssure after clonidine (Delta MAP 20.4+/-2.0 vs 9.7+/-2.8 mmHg; P<0.05) . No variations were detected in hyperthyroid patients after therapy e ither in basal hormones levels or in the magnitude of decrement in MAP and noradrenaline induced by clonidine. CONCLUSIONS We conclude that in spite of the previously reported abnormalities in alpha(1) and beta -adrenergic receptor activity, the inhibitory alpha(2)-receptor pathwa y is normal in patients with altered thyroid function.