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Increased Circulating Atrial Natriuretic Peptide in Patients With Thyrotoxicosis

Masakazu Kohno, MD; Toshifumi Matsuura, MD; Kenichi Yasunari, MD; Mitsutaka Yasuda, MD; Takanao Takeda, MD; Yoshiki Nishizawa, MD; Hirotoshi Morii, MD
Arch Intern Med. 1986;146(10):2077. doi:10.1001/archinte.1986.00360220259043.
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To the Editor.  —We have recently shown that the release of atrial natriuretic peptide (ANP) is chronically stimulated in experimental hyperthyroid rats produced by L-thyroxine administration, and is suppressed in hypothyroid rats produced by propylthiouracil administration.1 In the present study, we measured plasma ANP levels in six patients with moderate or severe thyrotoxicosis before and after successful treatment with methimazole (dosage, 20 to 40 mg/d; duration, four to 16 weeks). Patients with congestive heart failure were excluded, as plasma ANP levels were found to be high in this state.2 Plasma ANP levels were measured according to the method previously reported.1,3Plasma atrial natriuretic peptide (ANP) level, serum thyroxine level (T4), blood pressure (BP), and heart rate (HR) in patients with thyrotoxicosis before and after successful treatment with methimazole. The hatched area is the normal range (mean A±2 SD).Plasma ANP levels, serum thyroxine levels, blood pressures, and heart rates before and after the treatment

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