No specific organ removes atrial natriuretic peptide from the human plasma.

The fate of atrial natriuretic peptide (ANP) was studied by arterial and venous catheterization in ischemic heart disease patients, and arterio-venous blood sampling in healthy kidney donors at the time of transplantation. In vitro ANP degradation was examined using healthy human plasma. In ischemic heart disease, the plasma ANP concentration at the inferior vena cava was 62.6% of that at the left ventricle, and that at the superior vena cava was 82.8%. Arterio-venous gradients were similar from pulmonary artery to vein (88.3%), from celiac artery to the hepatic vein (75.5%) and from the femoral artery to vein (85.4%). In the donor for kidney transplantation, renal arterio-venous gradient was also similar at 77.1%. No platelet consumption of ANP was noted, and the molecular forms of ANP present in the circulation were similar in samples obtained from both the coronary sinus and the superior or inferior vena cava. We conclude that no specific organ plays a dominant role in ANP degradation, and that ANP molecular forms may not be altered during circulation.