Normalization of thyroid hormone levels in patients with either hyper- or hypothyroidism results in a profound change of atrial natriuretic peptide (ANP) levels

Abstract

Atrial Natriuretic Peptide (ANP) is a hormone produced by cardiac atrial myocytes. Thyroid hormones may affect its release. The aim of this study was to analyze the effect of hyper and hypothyroidism on the secretion of ANP and its relationship with the changes of the renin-angiotensinaldosterone system. Plasma ANP concentration as well as plasma renin activity (PRA) and aldosterone (ALDO) were measured in 21 patients with hyperthyroidism, 12 patients with hypothyroidism and 29 normal controls. Moreover, in 5 hyperthyroid and 8 hypothyroid patients hormones measurements were performed at diagnosis and 15, 30, 45 and 60 days after starting the appropriate therapy. Statistical analysis was performed employing the Wilcoxon two sample test to compare the ANP levels in normal and hyper or hypothyroid patients while the pairwise comparisons were evaluated using the Spermans rank correlation. Partial correlation and regression models were used to examine the joint effects of multiple predictors on ANP. ANP levels were significantly higher in hyperthyroid (mean±SEM, 17±1.7pmol/L, p<0.001) and lower in hypothyroid patients (6.18±1.14pmol/L, p<0.01) compared to normals (10.35±0.59pmol/L). In the hyperthyroid patients following treatment with antithyroid drugs plasma ANP levels reached normal values after 15 days and remained stable thereafter. In the hypothyroid patients, ANP levels increased gradually following initiation of treatment with thyroxine, reaching values comparable to controls at day 45. PRA was significantly higher only in hyperthyroid patients compared to controls. ALDO concentrations were not different in all groups studied. No correlation was found between plasma ANP levels and T3, T4, TSH, PRA and ALDO levels in the individual groups, while a positive correlation for T3 (r=0.610, p<0.01), T4 (r=0.653, p<0.01) and pulse rate (r=0.704, p<0.01) and negative correlation with TSH (r=-0.519, p<0.01) was found when all groups were pooled together. In conclusion, our data indicate that thyroid hormones affect positively ANP secretion from cardiac myocytes. This effect may be, at least in part, indirect via hemodynamic alterations.

Effects of thyroid hormones on the heart

“…These changes result in preload increase and afterload reduction, leading to a significant increase in stroke volume. 23,24 A higher cardiac preload may trigger secretion of atrial natriuretic peptide (ANP); however, it is suggested that TH-induced myocardial ANP secretion in healthy subjects is not the result of a direct action on the myocardium, but rather the result of an indirect modification in cardiovascular hemodynamic leading to increased atrial stretch. Therefore, hyperthyroidism is characterized by a high cardiac output state with a remarkable increase in heart rate and cardiac preload and a reduction in peripheral vascular resistance, resulting in hyperdynamic circulation (Fig.…”

Serum Concentrations of BNP and ANP in Patients with Thyrotoxicosis

“…Furthermore, it has been shown that the production of ANP is increased by hormonal factors including thyroid hormone. Actually, hyper-or hypothyroidism is associated with altered serum ANP levels [6][7][8][9][10][11].…”

Protective actions of human tissue kallikrein gene in transgenic rat hearts

“…ANP is a hormone produced by cardiac atrial myocytes and thyroid hormones may affect its release. Koukoulis et al studying the effect of hyper and hypothyroidism on the secretion of ANP found that thyroid hormones affect positively ANP secretion from human cardiac myocytes [11]. Moreover, is well known that plasma ANP is elevated in several pathological conditions, including valve disease, coronary heart disease and cardiomyopathy [12].…”