Heart with circulatory failure secretes and processes atrial natriuretic peptide in a manner different from normal heart

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Abstract
The role of catecholamine in atrial natriuretic peptide (ANP) secretion and its secretory mechanism in normal humans is not well defined; therefore, we studied the relationship among ANP, catecholamine, and atrial pressures in 25 patients without cardiovascular disease and in 35 patients with chronic congestive heart failure (CHF, 20 in mitral valve disease and 15 in dilated cardiomyopathy). In patients without cardiovascular disease, right atrial pressure at rest showed a positive correlation (r = 0.80, p>0.001) with ANP concentration, whereas left atrial pressure did not. The relation narrowed (r = 0.82) when the bicycle ergometer exercise in the supine position was conducted. Neither adrenalin nor noradrenalin significantly correlated with ANP concentration. In patients with mitral valve disease and dilated cardiomyopathy, the significant relations (r = 0.56 p>0.001, r = 0.85 p>0.001, respectively) between left atrial pressures and ANP concentrations at rest were observed, and following exercise, induced more significant relations. Right atrial pressures did not correlate positively with ANP concentrations. The increments of ANP concentrations induced by exercise load were markedly reduced compared with those of patients without cardiovascular disease. Although concentrations of both noradrenalin and adrenalin in patients with mitral valve disease and dilated cardiomyopathy at rest were much higher than those without cardiovascular disease, only noradrenalin had a highly positive correlation with ANP concentrations (r = 0.88 p> 0.001, r = 0.78 p>0.001, respectively). Furthermore, the circulating ANP molecular weight forms in all patients studied were analyzed by gel chromatography coupled with radioimmunoassay. In contrast to the predominant form of α‐ANP in patients without cardiovascular disease, larger molecular forms occurred in most patients with CHF. We conclude that ANP secretion from the heart of patients with CHF is regulated not only by atrial pressure but noradrenalin, and that its processing mechanism is different from that of the normal heart.