Release of atrial natriuretic peptide during pulmonary artery clamping in man.

The vasodilating hormone atrial natriuretic peptide (ANP) is secreted from the heart in response to atrial wall stretch, but knowledge of the time course of ANP secretion after acute releasing stimuli is limited. The time from stimulus to release of immunoreactive atrial natriuretic peptide (irANP) was investigated by unilaterally clamping the pulmonary artery in 12 patients undergoing pulmonary surgery. The second messenger to ANP-induced vascular relaxation, plasma cyclic guanosine monophosphate (p-cGMP), was measured as an indirect marker of the vascular effects of ANP. Immediately after applied clamping, p-irANP (baseline level 15.4 +/- 2.9 pmol l-1) started to increase, reaching a significant, although moderate, increase (11 +/- 4%, P < 0.05) after 2 min. This elevation of p-irANP remained during the entire clamping period (+13 +/- 6%, P < 0.05 vs. baseline). Within 1 min of declamping, p-irANP returned to the baseline level. No conclusive alterations in p-cGMP were observed. The prompt ANP response to the applied stimulus, and the return to baseline after declamping, may indicate the presence of a short time-acting releasing mechanism of ANP.