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In 1988, a Japanese group isolated B-type (or brain) natriuretic peptide (BNP) from porcine brain extracts by monitoring its relaxant effects on chick rectum.1 Since then studies in humans and rodents demonstrated that BNP is a cardiac hormone mainly expressed in the heart, where its concentration is considerably higher than in brain. BNP possesses a 17-amino acid ring structure containing two cysteine residues, which is essential for its biological activity. Mechanical stress, ischaemia, cytokines and neurohumoral factors, including angiotensin II, stimulate expression of BNP (figure 1),2 and levels of myocardial BNP mRNA and circulating BNP and N-terminal proBNP (NT-proBNP) are markedly increased in patients with congestive heart failure.2 BNP is therefore considered to function as an emergency defence against ventricular overload in disease states.
Funding This study was supported in part by Scientific Research Grants-in-Aid 20590837 and 23591041 from the Ministry of Education, Culture, Sports, Science and Technology of Japan (to TN); a grant (AS 232Z01302F) from the Japan Science and Technology Agency (to TN); a grant from the Suzuken Memorial Foundation (to TN) and the Intramural Research Fund of National Cerebral and Cardiovascular Center (to NM).
Competing interests None.
Contributors TN mainly wrote the manuscript. YN, KK, and NM criticised it and provided the useful discussion.
KN and KK are supervisors and they provided useful comments to the manuscript.
Provenance and peer review Not commissioned; internally peer reviewed.
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