Brain Natiruretic Peptide in IntensiveCare Unit

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.