Brain natriuretic peptide (BNP) levels are simple and objective measures of cardiac function. These measurements can be used to diagnose heart failure, including diastolic dysfunction
- 32 AA Natriuretic peptide released by Ventricular stretch
- Synthesized, sored and released by the cardiac ventricles (as well as brain).
- Proteolysis of pro-BNP (108 amino acids) results in BNP (32 amino acids) and the N-terminal piece of pro-BNP (NT-pro-BNP; 76 amino acids).
- Both BNP and NT-pro-BNP are sensitive, diagnostic markers for heart failure in patients.
- Increases GFR by Dilation of afferent arteriole and Constriction of efferent arteriole
- Decreases sodium reabsorption by closing sodium
channels in the apical membrane
- Overall effect: increased sodium excretion
Levels: Read NT-proBNP for BNP
- BNP level correlates with LV pressure, degree of dyspnoea, and state of neurohormonal modulation.
- BNP synthesis is increased by thyroid hormones as well as glucocorticoids, endothelin-1, angiotensin-II and tachycardia, independent of the haemodynamic effects of these factors.
- BNP is a useful marker for heart failure. Measurement of plasma BNP concentration is evolving as a very efficient and cost-effective mass screening technique for identifying patients with various cardiac abnormalities regardless of aetiology and degree of LV systolic dysfunction
- BNP causes increased glomerular filtration rate (GFR) and inhibition of sodium reabsorption leading to natriuresis and diuresis.
- BNP leads to reduced blood pressure, and reduced pre-load due to relaxing effects on vascular smooth muscle.
Other causes of high BNP or NT-proBNP for BNP
- Renal failure, pulmonary hypertension, sepsis
- Valvular disease, atrial fibrillation and acute coronary syndrome