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  • Title: Serum angiotensin-converting enzyme and plasma atrial natriuretic peptide levels in hyperthyroid and hypothyroid rabbits.
    Author: Yeğin E, Yiğitoğlu R, Ari Z, Celik I, Akçay F, Süzek H.
    Journal: Jpn Heart J; 1997 Mar; 38(2):273-9. PubMed ID: 9201114.
    Abstract:
    BACKGROUND: It is known that serum angiotensin-converting enzyme (ACE), and plasma atrial natriuretic peptide (p-ANP) levels increase in hyperthyroidism. However, the precise mechanism of the effects of thyroid hormone on ANP release remains to be clarified. No study investigating serum ACE together with p-ANP levels has been performed in experimental hyperthyroid and hypothyroid rabbits. The present study was designed in order to provide additional evidence of increased ANP production and secretion in hyperthyroidism and to investigate the relationships between ANP, ACE and thyroid hormones. METHODS: Male New Zealand white rabbits (2.3-3.4 kg) were used throughout the study. Hyperthyroidism was induced by daily intraperitoneal administration of L-thyroxin (50 micrograms/100 g). Hypothyroidism was induced by daily intraperitoneal injection of propylthiouracil (2 mg/100 g body weight). Twelve days after the end of treatment, animals were sacrificed under anesthesia and blood samples were obtained from the aorta for serum ACE and thyroid hormone and p-ANP determinations. RESULTS: Serum ACE, plasma renin activity (PRA) and p-ANP were higher in hyperthyroid rabbits and lower in hypothyroid rabbits than in euthyroid rabbits. ANP concentration in atria was lower in hyperthyroid rabbits and higher in hypothyroid rabbits than in euthyroid rabbits. p-ANP, PRA and serum ACE levels were positively correlated with serum thyroxin levels. Inverse correlation was found between serum thyroxin and ANP concentration in atria (a-ANP), and between p-ANP and a-ANP. CONCLUSIONS: Our results indicate that not only p-ANP but also serum ACE activity was markedly increased in experimental hyperthyroid rabbits. It was thought that there were both direct and indirect effects of thyroxin on the release of ANP.
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