The circulatory effects of beta type natriuretic peptides

Atrial Natriuretic Peptide: Atrial natriuretic peptide (ANP) is mainly secreted from atria in response to excessive stretch (volume expansion).  It is a 28 amino acid polypeptide.  It attaches to cell membrane receptors with subsequent activation of guanylyl cyclase.

          ANP is a direct vasodilator.  ANP increases water (diuresis) and sodium excretion (natriuresis) by the kidney due to effects both on the glomerulus and the tubule.  Hypervolemia triggers ANP secretion e.g. heart failure, renal failure.  Furthermore, ANP serum levels will return to normal with successful therapy of the hypervolemic state.

 

Brain Natriuretic Peptide: Brain natriuretic peptide (BNP) was initially identified in the brain but is also present in the heart, particularly the ventricles.  It is a 32 amino acid polypeptide secreted by the ventricles in response to excessive myocardial stretch.  The circulating concentration of BNP is less than 20 percent of that of ANP in normal subjects, but can equal or exceed that of ANP in patients with congestive heart failure.

          BNP is a vasodilator and thus decreases systemic vascular resistance.  BNP also increases salt excretion by the kidney (natriuresis).

          The effects of ANP and BNP are a fall in systemic blood pressure, an increase in cardiac output and a decrease in blood volume.  They also both inhibit the renin-angiotensin system as well as systemic and renal sympathetic activity.

          The release of both ANP and BNP is increased in heart failure due to the high filling pressures. The plasma concentrations of both hormones are high in asymptomatic and symptomatic left ventricular dysfunction, permitting their application not only in diagnosis but also prognosis of heart failure.

          BNP may have a therapeutic role in heart failure due to its hemodynamic effects.  The drug, nesiritide (recombinant human BNP), has been approved for the therapy of acute decompensated heart failure.  Its full application will not be discussed here.

 

JG Augoustides, M.D.

Associate Professor of Anesthesiology and Critical Care

University of Pennsylvania