الفهرس 
Physiology and history of BNPOnly 14 pages are availabe for public view
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Abstract
BNP was first isolated from porcine brain extracts in 1988 by Sudoh et al. Soon after its discovery, however, the highest concentrations of BNP were shown to be in the heart, where it acts as a cardiac hormone.
Infusions of brain natriuretic peptide at doses that raise their plasma concentrations slightly above normal result in diuresis and natriuresis, unrelated to changes in blood pressure. These infusions reduce plasma renin and aldosterone concentrations and inhibit angiotensin II–stimulated aldosterone secretion.
(BNP) is a neurohormone secreted from the myocytes mainly in response to increased wall tension such as volume or pressure overload. The levels also increase during states of haemodynamic stress, e.g. left ventricular hypertrophy, ventricular dilatation, in heart failure, acute coronary syndromes and AF as well as with ageing, renal dysfunction, and female gender.
Close monitoring of body fluid status is mandatory for patients with advanced CKD because failure to do so results in acute cardiopulmonary decompensation. Therefore, measuring therapies that decrease left ventricular wall tension, such as reducing body fluid volume using diuretics, dialysis, angiotensin-converting enzyme inhibition, erythropoietin or a beta-blockade, are of the most potential value in patients with CKD and elevated BNP levels.
BNP may be elevated in patients with right ventricular pressure overload due to pulmonary arterial hypertension, pulmonary thromboembolism, undifferentiated chronic lung disease and respiratory failure where they are also associated with a poor prognosis.
Sepsis is common in clinics with a high mortality and poor prognosis. In recent years, BNP have been applied in predicting the prognosis of patients with severe sepsis or septic shock.