Ozone increases amino‐ and carboxy‐terminal atrial natriuretic factor prohormone peptides in lung, heart, and circulation

Abstract

Ozone can cause pulmonary edema and simultaneously decrease blood pressure. Atrial natriuretic peptides may mediate both of these effects in that they increase pulmonary capillary permeability resulting in edema formation and are potent vasodilating peptides. To examine this possibility, the lungs of Fischer 344 rats were exposed to ozone (0.5 ppm) for 8 hours which resulted in a three- to fourfold increase in atrial natriuretic peptides. Ozone also increased atrial natriuretic peptides in the heart two- to fivefold from 266 +/- 25, 226 +/- 22, and 288 +/- 40 ng/g (room air) to 716 +/- 26, 471 +/- 14, and 1473 +/- 235 ng/g recognized by the proANFs 1-30 and 31-67 and atrial natriuretic factor radioimmunoassays, respectively. Ozone also doubled the concentrations of pro-ANFs 1-30, 31-67, and 1-98 and ANF in the circulation. This study demonstrates that ozone increases atrial natriuretic peptides within the heart, lung, and circulation, suggesting that atrial natriuretic peptides may mediate the decreased blood pressure and pulmonary edema observed with ozone exposure. Since the proANF 31-67 radioimmunoassay exclusively recognizes the ANF prohormone within the heart, this study further indicates that ozone can increase the synthesis of the ANF prohormone.