This Article Full Text (PDF) Submit a related Letter to the Editor Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Copyright Permission Citing Articles Citing Articles via Google Scholar Google Scholar Articles by ANDO, K. Articles by MARUMO, F. Search for Related Content PubMed PubMed Citation Articles by ANDO, K. Articles by MARUMO, F.

Circulating Forms of Human Atrial Natriuretic Peptide in Patients with Congestive Heart Failure^*

Second Department of Internal Medicine, Tokyo Medical and Dental University (K.A., Y.H., T.E., M.S., F.M.) Tokyo 113, Japan
Kitasato Biochemical Laboratories (K.A.) and Department of Medicine, Kitasato University School of Medicine (T.K., K.S.) Sagamihara 228, Japan

Address requests for reprints to: Dr. Yukio Hirata, Endocrine Division, Second Department of Internal Medicine, Tokyo Medical and Dental University, 1–5–45 Yushima, Bunkyo-ku, Tokyo 113, Japan.

To elucidate the circulating forms of human atrial natriuretic peptide (hANP) in patients with congestive heart failure (CHF), plasma samples obtained from 36 patients with CHF were analyzed and compared with those from normal subjects. Plasma concentrations of hANP-like immunoreactivity (LI) from normal subjects and patients with mild CHF (class I), as classified by the New York Heart Association (NYHA) functional criteria, did not differ (15 ± 1 vs. 16 ± 1 pmol/L, mean ± SE), whereas plasma levels of hANP-LI in patients with moderate and severe CHF significantly (P < 0.01) increased in relation to the severity of CHF (class II, 44 ± 4 pmol/L; class III, 116 ± 24 pmol/L; class IV, 141 ± 21 pmol/L).

Reverse-phase HPLC and gel permeation chromatography coupled with RIA for hANP revealed that the circulating forms of hANP-LI consisted of -hANP, β-hANP, and -hANP in CHF, whereas -hANP predominated in normal plasma. The percentage of β-hANP in total hANP-LI as calculated from the chromatograms by gel filtration was greater in severe CHF (NYHA class III and IV) than those in mild CHF (NYHA class I and II), and apparently exceeded those of other forms. Successful medical treatment for CHF resulted in a marked reduction of total plasma hANP-LI levels with a concomitant disappearance or reduction of β-hANP in 14 patients examined.

These data suggest that β-hANP and -hANP are secreted from the failing human heart, possibly resulting from the augmented synthesis and/or the altered processing of hANP precursor in cardiocytes, and that circulating β-hANP may serve as a potential marker for the severity of CHF in man.

^* Supported in part by Research Grants (62A-1, 63C-1) for Cardiovascular Diseases from the Ministry of Health and Welfare and Grantsin-Aid (01480217, 01480286) for Scientific Research from the Ministry of Education, Science and Culture, Japan, and a fund from the Japan Cardiovascular Research Foundation (1989).

Received November 6, 1989.