Nitric oxide (NO) is present in the exhaled breath of humans and exper
imental animals, but its physiologic role and cellular source(s) remai
n to be determined. Possible sites of origin are pulmonary endothelial
cells and/or resident macrophages. Here we have tested the hypothesis
that changes in cardiovascular status can alter the apparent pulmonar
y excretion of NO. Exercise on a stationary bicycle produced rapid and
reversible increases in pulmonary NO excretion rate, and changes in N
O excretion rate during exercise were well correlated with observed ch
anges in heart rate. These results suggest that changes in expired NO
during exercise are related to corresponding cardiovascular responses.