Brain natriuretic Peptide (BNP)
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Brain natriuretic peptide (BNP), also known as B-type Natriuretic Peptide, brain natriuretic peptide, which is another member of the natriuretic peptide system after atrial natriuretic peptide (ANP). Because it was first separated from the pig brain in 1988 by the Japanese scholar Sudoh, in fact, it mainly comes from the ventricle. Like ANP, BNP has a ring structure composed of 17 amino acids through a pair of disulfide bonds, which is necessary for the binding of receptors, in which disulfide bonds are important for the bioactivity of BNP. BNP is species-specific. Rat BNP consists of 45 amino acids, while pig, dog and human BNP consists of 32 amino acids. The human BNP gene fragment is located at the distal end of the short arm of chromosome 1 and is connected to the upstream ANP fragment. Its reverse transcriptional deoxyribonucleic acid (cDNA) is composed of 1900 nucleotides, and the messenger ribonucleic acid (mRNA) of BNP is composed of 900 to 1000 nucleotides, which can be expressed as BNP precursor. The N-terminal signal peptide becomes (proBNP), a BNP precursor containing 108amino acids, but is not stored in secretory granules, but is mainly secreted from the ventricle. During its secretion or after entering the blood, it decomposes into bioactive BNP (C-terminal fragment containing 32 amino acids) and N-terminal fragment. The release of BNP was regulated by left ventricular extension and wall tension.
Mechanism of action
BNP has important pathophysiological significance. It can promote the excretion of sodium and urination, has a strong vasodilating effect, and can resist the vasoconstriction of renin-angiotensin-aldosterone system (RAAS). Like ANP, it is a major endocrine system to resist volume overload and hypertension. Cardiac dysfunction can greatly activate the natriuretic peptide system, and increased ventricular load leads to BNP release.
Cardiovascular function and clinical application of BNP
- Both BNP and ANP are natural antagonists of renin angiotensin aldosterone system (RAAS). They also resist the effects of vasopressin and sympathetic nerve on sodium and water retention and hypertension.
- At present, the clinical research on BNP is mainly focused on left ventricular dysfunction (LVD), where left ventricular function refers to systolic function. In both normal and LVD patients, BNP was mainly synthesized and secreted by left ventricular cardiomyocytes and returned to the interventricular septum vein to enter the circulation through the coronary sinus, and its secretion was mainly regulated by the tension of the left ventricular wall. The severity of LVD was positively correlated with its secretion. The level of BNP in peripheral blood could reflect the rate of ventricular secretion and the degree of LVD.
- The level of plasma BNP was positively correlated with the degree of LVD after AMI. BNP could accurately reflect the changes of regional ventricular wall tension after infarction, and the tension was affected by infarction area, left ventricular morphological changes, myocardial mechanical stress and other factors. Therefore, the measurement of plasma BNP in patients with myocardial infarction can predict the size of infarction area and left ventricular function at the same time.
In conclusion, with the deepening of the study, the determination of plasma BNP concentration is likely to be an important supplement to the evaluation of cardiac function, and become a simple and convenient routine examination.
1. Mukoyama, M., Nakao, K., Hosoda, K., Suga, S., Saito, Y., Ogawa, Y., ... & Yasue, H. (1991). Brain natriuretic peptide as a novel cardiac hormone in humans. Evidence for an exquisite dual natriuretic peptide system, atrial natriuretic peptide and brain natriuretic peptide. The Journal of clinical investigation, 87(4), 1402-1412.
2. Calzetta, L., Orlandi, A., Page, C., Rogliani, P., Rinaldi, B., Rosano, G., ... & Matera, M. G. (2016). Brain natriuretic peptide: Much more than a biomarker. International journal of cardiology, 221, 1031-1038.