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α2‐Adrenergic activity is normal in patients with thyroid disease
Author(s) -
Rio Graziano,
Zizzo Giuseppe,
Marrama Paolo,
Venneri Maria Grazia,
Casa Luciano Delia,
Velardo Antonino
Publication year - 1994
Publication title -
clinical endocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.055
H-Index - 147
eISSN - 1365-2265
pISSN - 0300-0664
DOI - 10.1111/j.1365-2265.1994.tb02474.x
Subject(s) - clonidine , medicine , endocrinology , blood pressure , basal (medicine) , thyroid , adrenergic , catecholamine , sympathetic nervous system , agonist , receptor , diabetes mellitus
Summary OBJECTIVE Several studies indicate an inverse relationship between the sympathetic nervous system activity and thyroid function. Altered adrenoceptor sensitivity, particularly α and β, have been described in hypothyroid and hyperthyroid patients. No information in patients with thyroid disease is available on the main mechanism regulating sympathetic nervous system outflow, i.e. the α 2 ‐adrenoceptor pathway. In our study we evaluated α 2 ‐adrenergic activity in patients with thyroid disease by the assessment of cardiovascular and catecholamine response to clonidine, a central a 2 adrenergic agonist. PATIENTS Ten patients with hypothyroidism, six patients with hyperthyroidism 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 μg/kg body weight of clonidine. Blood pressure and pulse rate were measured 30,60,90,120,130 and 140 minutes after clonidine administration; blood samples for determination of catecholamines were drawn at 120,130 and 140 minutes. RESULTS At presentation the decrease in plasma noradrenaline 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 differences were detected in the fall in adrenaline and mean arterial pressure (MAP) after clonidine. The adequate therapy induced in hypothyroid patients a decrease in the basal levels of noradrenaline (1.88±0.28 vs 0.67±0.10 nmol/l; P <0.05) and a lesser fall in mean arterial pressure after clonidine (AMAP 20 4 ± 2 0 vs 9.7 ±2.8 mmHg; P < 0.05). No variations were detected in hyperthyroid patients after therapy either 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 α 1 and β‐adrenergic receptor activity, the inhibitory α 2 ‐receptor pathway is normal in patients with altered thyroid function.