Atrial natriuretic peptides in pathophysiological diseases

A molecular variant in exon 1 of atrial natriuretic peptide prohormone gene is associated with a 2-fold increased risk of stroke. The gene product of exon 1, i.e., long acting natriuretic peptide [LANP] is a physiological regulator of blood pressure based upon antisera to LANP causing a significant increase in blood pressure in both normotensive and in spontaneously hypertensive animals. These data taken together suggest that the single amino acid change in LANP may contribute to cerebrovascular accidents. In salt and water retaining states such as congestive heart failure and cirrhosis with ascites, atrial natriuretic peptides increase proportionally in the circulation to the severity of the sodium and water retention. Their increase is in an apparent attempt to overcome the sodium and water retention. One of the atrial natriuretic peptides, i.e., vessel dilator, enhances urine flow 2-13-fold and sodium excretion 4-fold while decreasing systemic vascular resistance 24% and increasing cardiac output 34% in CHF individuals. Vessel dilator markedly improves acute tubular necrosis even when given 2 days after an acute renal ischemia and reduces mortality from 88 to 14% in an animal model of acute renal failure.